Jiang 2019
Jiang 2019
Jiang 2019
2, 2019 395
Spices and herbs have been in use for centuries for their medicinal benefits is fully acknowledged, and there
both for culinary and medicinal purposes. Spices is a growing amount of literature concerning the potential/
not only enhance the flavor, aroma, and color of purported benefits of these foods from a health perspective.
food and beverages, but they can also protect These benefits include their possible role in conferring
from acute and chronic diseases. More Americans protection against cardiovascular and neurodegenerative
are considering the use of spices and herbs for diseases, cardiovascular disease, cancer, and type 2 diabetes
medicinal and therapeutic/remedy use, especially mellitus (T2DM; 1–3).
for various chronic conditions. There is now Spices and herbs have been extensively studied in different
ample evidence that spices and herbs possess countries because of their beneficial effects on human health
antioxidant, anti-inflammatory, antitumorigenic, (1, 4). However, the interest in spices has only recently grown
anticarcinogenic, and glucose- and cholesterol- in the Western world (5, 6). Greater awareness of ethnic spices
lowering activities as well as properties that for disease prevention and health promotion is needed in this
affect cognition and mood. Research over the population.
past decade has reported on the diverse range
of health properties that they possess via their Use and Knowledge of Spices and Herbals
bioactive constituents, including sulfur-containing
compounds, tannins, alkaloids, phenolic The U.S. Department of Agriculture reports that the
diterpenes, and vitamins, especially flavonoids consumption of spices in the United States has climbed
and polyphenols. Spices and herbs such as clove, exponentially over the course of the last half-century, with spices
rosemary, sage, oregano, and cinnamon are such as ginger and chili pepper being used more frequently than
excellent sources of antioxidants with their high ever before (6). According to the U.S. National Health and
content of phenolic compounds. It is evident that Nutrition Examination Survey, 5–10% of adults in the United
frequent consumption of spicy foods was also States use botanical supplements such as spices, for health
linked to a lower risk of death from cancer and benefits (7, 8). Such increased use could in part be because of
ischemic heart and respiratory system diseases. the lack of side effects from spices, greater availability than
However, the actual role of spices and herbs in the traditional medicines, and the consideration of known health
maintenance of health, specifically with regards benefits of spices (6–8).
to protecting against the development of chronic, It is evident that more Americans are considering the use of
noncommunicable diseases, is currently unclear. spices and herbs for medicinal and therapeutic uses, especially
This review highlights potential health benefits of to remedy various chronic conditions, reduce disease symptoms,
commonly used spices and herbs such as chili and aid in treatment and management of common health
pepper, cinnamon, ginger, black pepper, turmeric, problems. A recent cross-sectional survey study involving 703
fenugreek, rosemary, and garlic. adults in the Midwestern United States examined consumers’
perceptions about spices and their use and predictors of spice
use (9) found that almost half of the participants were interested
S
pices have been an integral part of culinary culture in learning about health benefits of spices (48%) and were
around the world and have a long history of use for willing to use spices as complementary and alternative medicine
flavoring, coloring, and preserving food, as well as for therapies (51%). Most (>50%) of the participants were familiar
medicinal purposes. The increased use of spices as flavorings with or had used 8 out of the 10 listed spices. The majority
in foods is a major trend worldwide (1). Spices not only of participants (54%) was currently using one or more spices
enhance the flavor, aroma, and color of food and beverages, on a daily basis and believed that ginger (64%), garlic (58%),
but they may also protect against the development of acute and cinnamon (56%) could promote good health and wellness
and chronic, noncommunicable diseases and help people (Table 1). Furthermore, the majority of the participants listed
maintain health. The long historical use of herbs and spices 7 out of 10 spices as effective in preventing a specific disease
with ginger (72%), garlic (68%), and cinnamon (67%) listed as
effective by more than two-thirds of the participants. In addition
to the adult population use, spices have also been explored
Guest edited as a special report on “Authentication, Quality, in pediatric populations. For example, more than 1/10 of the
Health, and Regulation of Spices and Herbs” by Paul Ford and Milda
Embuscado
infants and children were given spices, primarily to remedy
Corresponding author’s e-mail: [email protected] minor ailments such as fussiness or stomach complications,
DOI: https://doi.org/10.5740/jaoacint.18-0418 coughs, and colds.
396 Jiang: Journal of AOAC International Vol. 102, No. 2, 2019
Table 1. Perceived efficacy of spices in promoting health foods almost every day had a relative 14% lower risk of death
and wellness (9) compared with those who consumed spicy foods less than once a
week. It was found that frequent consumption of spicy foods was
Effective na
Spice b
(% agreement) also linked to a lower risk of death from cancer, ischemic heart
diseases, and respiratory diseases, and this was more evident in
Ginger 450 (64) women than in men. People who consumed fresh chili tended to
Garlic 404 (58) have a lower risk of death from cancer, ischemic heart disease,
Cinnamon 392 (56) and diabetes (16, 17).
Chili pepper 300 (43) In addition, subjects with a high spice preference had a lower
salt intake and blood pressure than subjects who disliked spicy
Turmeric 251 (36)
food. The enjoyment of spicy flavors enhanced salt sensitivity
Cilantro 168 (24)
and reduced salt preference. Salt intake and salt preference
Cloves 163 (23) were related to the regional metabolic activity in the insula
Black pepper 163 (23) and orbitofrontal cortex (OFC) of participants. A more recent
Curry leaves 108 (15) multicenter, double-blind observational and interventional
Fenugreek 76 (11)
study showed that administration of capsaicin, the major spicy
a
component of chili pepper, enhanced the insula and OFC
n = 703. metabolic activity in response to high-salt stimuli, which reversed
b
% = Percent of individuals who believe that a certain spice can
promote health and wellness.
the salt intensity-dependent differences in the metabolism of
the insula and OFC (18). It was concluded that enjoyment of
spicy foods may significantly reduce individual salt preference,
Biological Activities of Spices and Herbs Constituents daily salt intake, and blood pressure by modifying the neural
processing of salty taste in the brain. Application of spicy flavor
Culinary herbs and spices are foods that are a rich source may be a promising behavioral intervention for reducing high
of bioactive molecules such as sulfur-containing compounds, salt intake and blood pressure.
tannins, alkaloids, phenolic diterpenes, and vitamins, especially
flavonoids and polyphenols (4, 10). Spices and herbs such as Overview of Selected Herbs and Spices
clove, rosemary, sage, oregano, and cinnamon are excellent
sources of antioxidants with their high content of phenolic Chili Pepper
compounds (10, 11).
Research over the past decade has reported that bioactive Bioactive components.—Red pepper contains 0.2–2%
constituents of spices possess the diverse range of health benefits capsaicinoids, which are responsible for the pungency or bite in
(1, 5, 11, 12). There is now ample evidence that culinary herbs capsicums. Capsaicin, an alkaloid, accounts for about 50–70%
and spices are sources of constituents that possess antioxidative, of the total capsacinoids and dihydrocapasaicin for 20–25%,
anti-inflammatory, antitumourigenic, anticarcinogenic, and which, together with capasaicin, provides the fieriest notes from
glucose- and cholesterol-lowering activities as well as properties midpalate to throat. Red pepper also contains newly discovered,
that affect cognition and mood, which are actively used in nonpungent compounds called capsinoids (e.g., capsiate and
preclinical, clinical, and therapeutic trials investigating new dihydrocapsiate).
treatments of diseases. In addition, there is now a growing The beneficial effects of red pepper have long been
amount of literature on how polyphenols confer health benefits documented. The habitual consumption of spicy foods was
via their action on gut microbiota (13, 14), which, in humans, inversely associated with total and certain cause-specific
have been recently related to risks of diabetes, cardiovascular mortality (cancer, ischemic heart diseases, and respiratory
disease, liver cirrhosis, etc. diseases), independent of other risk factors of death. A
recent large population-based prospective study analyzed
the association between consumption of hot red chili peppers
Effect of Spices on Human Health and mortality, using a population-based prospective cohort
from the National Health and Nutritional Examination Survey
Culinary herbs and spices have been reported to have various III. The frequency of hot red chili pepper consumption was
beneficial effects on human health. There is ample research measured in 16 179 participants at least 18 years of age. Total
evidence to suggest that spice consumption is particularly related and cause-specific mortality were the main outcome measures.
to the reduced risk of mortality as a result of cancer, ischemic Total mortality for participants who consumed hot red chili
heart diseases, and respiratory diseases. A recent observational peppers was 21.6% compared with 33.6% for those who did
study assessed consumption of spicy foods as part of a daily diet not (absolute risk reduction of 12%; relative risk of 0.64).
and the total risk and causes of death in 487 375 participants, aged Consumption of hot red chili peppers was associated with
30–79 years, during a median follow-up of 7.2 years in China a 13% reduction in the instantaneous hazard of death. It is
and concluded that people eat spicy food to improve health (15). documented that the consumption of hot red chili pepper was
Compared with participants who ate spicy foods less than once a associated with reduced mortality. The findings are in line with
week, those who consumed spicy foods 1 or 2 days a week were previous evidence showing potential protective effects of spicy
at a 10% reduced risk of death (hazard ratios for death was 0.90). foods on human health (16).
And those who ate spicy foods three to five and six to seven days Antioxidant anti-inflammatory effects.—Red pepper capsaicin
a week were at a 14% reduced risk of death (the hazard ratios for has antioxidant potential in mitigating oxidative stress in various
death were both 0.86). In other words, participants who ate spicy tissues or organs in both in vitro and animal models (19–21).
Jiang: Journal of AOAC International Vol. 102, No. 2, 2019 397
Capsaicin-inhibited neutrophil (inflammatory cells) migration red pepper (C. annum; CH-19 sweet, a nonpungent cultivar of
toward the inflammatory focus reduced vascular permeability and red pepper, containing capsiate at 0.1 mg/kg dry weight) could
proinflammatory cytokine production in an animal study (21). enhance thermogenesis but have no impact on blood pressure
Capsaicin may also suppress obesity-induced inflammation by and heart rate (47, 48). A 12 week placebo-controlled human
modulating messenger molecules released by obese mice fat cells trial confirmed that consumption of capsinoids from C. annum
and inactivating macrophage to release proinflammatory mediators was associated with abdominal fat loss (49). Furthermore,
in vitro (22). Janssens et al. (50) investigated the 24 h effects of capsaicin
Cardiovascular health.—The antioxidant and antiplatelet on energy expenditure, substrate oxidation, and blood pressure
properties of capsaicin and the important role of capsaicin in during 25% negative energy balance and found that consuming
regulating energy metabolism may also contribute to its beneficial 2.56 mg capsaicin per meal supports negative energy balance
effects on the cardiovascular system (23–26). An animal study by counteracting the unfavorable negative energy balance effect
showed that 3 mg/kg/day capsaicin reduced low-density of decrease in components of energy expenditure as well as
lipoprotein (LDL) levels, increased high-density lipoprotein promotes fat oxidation in negative energy balance.
(HDL) levels, and reduced oxidative stress levels measured as Gut health.—Evidence suggests capsaicin is a gastroprotective
malondialdehyde in various tissues (27). In another animal study, agent in peptic ulcer disease (51, 52). Capsaicin inhibits
when capsaicin was used alone (0.015% in the diet) or combined acid secretion and stimulates alkali and mucus secretions
with curcumin, dietary high-fat–induced excess of triglycerides (particularly gastric mucosal blood flow), which help in the
in the blood was countered by 14 and 12%, respectively; the prevention and healing of ulcers (53). Red pepper sauce (which
total cholesterol was reduced 23 and 21%, respectively (28). is high in capsaicin) helps with issues swallowing by increasing
In addition, capsaicin preferentially inhibited arachidonic acid- the contractility and motility response of the human esophagus.
induced platelet aggregation in vitro (29). Capsaicin may also An acute administration of capsaicin seems to improve the
defend against heart disease via a transient receptor potential motor performance of the esophageal body in patients with
(TRP)-mediated modulation of coronary blood flow (30). Two ineffective esophagus motility (54).
randomized crossover intervention studies revealed 4 weeks of The antimicrobial activity of spices, has been highlighted
regular consumption of a chili blend (55% cayenne chili) at 16 g by inhibitory effects against Helicobacter pylori and other
a day increased the resistance of serum lipoproteins to oxidation bacteria and fungi (55, 56). Chili pepper has long been
and reduced resting heart rate. It also increased effective recognized to have a beneficial effect on the gut microbiota
myocardial perfusion pressure time in men but not women in humans. In recent years, rapidly emerging evidence has
(31, 32). A randomized, double-blind, placebo-controlled trial in implicated gut microbiota as a novel and important metabolic
44 pregnant women with gestational DM (GDM) documented factor that affects the health of the host (57), and several
that capsaicin-containing chili supplementation (5 mg/day studies in humans have related abundance, composition,
capsaicin) regularly improved postprandial hyperglycemia and and metabolites of gut microbiota to risk of obesity (58, 59),
hyperinsulinemia as well as fasting lipid metabolic disorders in diabetes (60), liver cirrhosis (61), and cardiovascular disease
women with GDM, and it decreased the incidence of large-for- (62). In a 6 week, controlled feeding trial, subjects were given
gestational-age newborns (33). the weight maintenance diet sequentially contained with
Blood glucose control.—Human trials found that 5 g or up to 10 mg/day capsaicin from chili powder (63). Dietary
more of chili pepper (Capsicum frutescens) was associated capsaicin increased the Firmicutes:Bacteroidetes ratio and
with a decrease in blood glucose level and maintenance of Faecalibacterium abundance, accompanied with increased
healthy insulin levels (34–36). Animal studies suggested that plasma levels of glucagon-like peptide 1 (GLP-1) and gastric
red pepper may affect insulin secretion from beta-cells and/or inhibitory polypeptide and decreased plasma ghrelin level.
peripheral insulin resistance, reduce liver glucose output and Further enterotype analysis revealed that these subjects could
increase glycogen (the main form of body fuel) storage, as well be clustered into Bacteroides enterotype (E1) and Prevotella
as activate the peroxisome proliferator-activated receptors in enterotype (E2), and the above beneficial effects were
vitro, which involve cell glucose and fat metabolism (37–39). mainly obtained in E1 subjects. Moreover, E1 subjects had
Furthermore, dietary capsaicin may provide beneficial effects significantly higher fecal Faecalibacterium abundance and
on glucose homeostasis via activating the TRP vanilloid type 1 butyrate concentration after capsaicin interventions than those
(TRPV1; 40). in E2 subjects.
Thermogenesis, satiety, and weight management.—Short-
term consumption of red pepper may have the potential to
assist in body weight management by increasing satiety and Cinnamon
fullness, reducing energy and fat intake, increasing body heat
production (thermogenesis), raising the body’s metabolic rate Bioactive components.—Cinnamon’s key components are
(41–43), preventing fat cells from growing into mature cells essential oils and other derivatives such cinnamaldehyde,
(adipogenesis; 44), and increasing the rate of fat burn-off (fat cinnamic acid and cinnamate (bark oil; 60–80%), eugenol
oxidation; 45). TRP channels, which are primary receptors for (leaf oil; 10%), and water soluble polyphenols (4–10%), e.g.,
pungent agents such as capsaicin, may in part be responsible catechin, epicatechin, procyanidin, quercetin, kaempferol,
for lipid catabolism and thermogenesis; activating of TRPV1 and polyphenolic polymers. The flavonoids are primarily
appears to stimulate cellular mechanisms against obesity (40). proanthocyanidins and oligomers of cinnamtannins. The doubly
Human studies suggest that red pepper enhances linked phenol type A polymers are believed to be the bioactive
thermogenesis and fat oxidation but also affect blood pressure component for glucose metabolism (64).
and heart rate (45–47). The longer-term use of capsaicin may be Antibacterial and antifungal activity.—Extracts of cinnamon
also limited by its strong pungency. However, a certain type of and its major components, cinnamaldehyde and eugenol, have
398 Jiang: Journal of AOAC International Vol. 102, No. 2, 2019
been shown to attack major respiratory and gastrointestinal tract hypoglycemic medications and other lifestyle therapies had
pathogens in vitro (65, 66). An anecdotal report suggests that modest effects on FPG and HbA1c (81).
cinnamon may have beneficial effects on chronic salmonella Proanthyocyanidins are considered active ingredients in
infection (67). Further, an in vitro study suggested cinnamon cinnamon aqueous extracts. Preclinical animal studies provide
may have some bactericidal activity against H. pylori (68), but evidence that components of cinnamon may decrease blood
there is a lack of evidence to support the use of cinnamon for glucose levels and increase insulin sensitivity (85). Cinnam
H. pylori infection eradication in humans. aldehyde is another active component derived from cinnamon.
Anti-inflammatory and antioxidant effects.—Cinnamon Accumulating evidence supports the notion that cinnamaldehyde
polyphenol extract suppressed inflammation processes through exhibits blood glucose-lowering effects in diabetic animals
the regulation of anti- and proinflammatory gene expression by increasing glucose uptake and improving insulin sensitivity
in vitro (69, 70). Cinnamaldehyde-inhibited cyclooxygenase-2 in adipose and skeletal muscle tissues, improving glycogen
(COX-2) and inducible nitric oxide synthase (iNOS), two major synthesis in liver, restoring pancreatic islets dysfunction,
inflammation systems (70). In a double-blind, placebo-controlled slowing gastric emptying rates, and improving diabetic renal
trial involving 22 overweight subjects with impaired fasting and brain disorders (86). Cinnamaldehyde exerts these effects
blood glucose, 500 mg/day aqueous extract of cinnamon (high through its action on multiple signaling pathways, including
in type A polyphenols) for 12 weeks reduced oxidative stress as PPARs, AMPK, PI3K/IRS-1, RBP4-GLUT4, and ERK/
measured by plasma malondialdehyde (MDA) levels (71). JNK/p38MAPK, TRPA1-ghrelin, and Nrf2 pathways (87).
Cardiovascular health.—Cinnamon and cinnamon extract Additionally, obese mice fed for 5 weeks with a cinnamon-
(high in type A polyphenols) lowered sugar-induced blood containing diet significantly reduced their cumulative body
pressure increase in one study with rats predisposed to weight gain and improved glucose tolerance without detectable
hypertension (72). Cinnamaldehyde has been reported to modification of insulin secretion (87).
inhibit platelet aggregation in vitro in human and rabbit cells Although evidence of glucose control in humans is
as well as reduce blood clots formed within a blood vessel in inconsistent, there is evidence of dose-related hypoglycemic
an animal study (73). By regulating gene expression involving effects. Recent human studies showed that cinnamon
inflammatory, insulin, and lipoprotein metabolism signaling supplements of 3 g/day or more had improved glucose control
pathways, a cinnamon extract (high in type A polyphenols) and insulin sensitivity in both healthy and diabetic subjects
inhibited the overproduction of lipoproteins and serum (88–92). In addition, consuming 500 mg/day aqueous extract of
triglycerides after a meal, suggesting that this extract may cinnamon (approximately 10 g cinnamon ground powder/day)
be beneficial in the control of lipid metabolism (74–76). In a for 12 weeks led to improvements in several metabolic features
recent systematic review and meta-analysis, Maierean et al. (77) (i.e., fasting blood sugar, SBP, and body composition; 93).
assessed 13 randomized controlled trials with 750 participants However, most human studies did not show any improvements
investigating the effect of cinnamon supplementation on blood in blood glucose control or insulin sensitivity when cinnamon
lipid concentrations. Cinnamon supplementation significantly was used at <3 g/day doses (92, 94–97).
reduced blood triglycerides and total cholesterol concentrations Hepatoprotective effect.—One study found the ethanol
without any significant effect on LDL-cholesrterol (LDL-C) extract of cinnamon showed hepatoprotective action against
and HDL-cholesterol (HDL-C). Moreover, cinnamon may have carbon tetrachloride–induced lipid peroxidation and liver
protective effects against metabolic syndrome aspects in various injury in rats by elevating antioxidant enzyme activities (98).
ways, and the use of cinnamon can be effective in reducing Cinnamon bark extract reduced the hepatic lipid accumulation
metabolic syndrome complications (78, 79). Consumption of and protected the liver from acute alcohol-induced fatty liver in
cinnamon (short term) is associated with notable reductions mice (99).
in systolic blood pressure (SBP) and diastolic blood pressure Neuroprotective property.—Various cinnamon species
(DBP; 80). and their biologically active ingredients have renewed
Blood glucose control.—The consumption of cinnamon is the interest toward the treatment of patients with mild-to-
associated with a statistically significant decrease in fasting moderate Alzheimer’s disease (AD) through the inhibition of
plasma glucose (FPG) levels. Cinnamon thus has been suggested tau protein aggregation and the prevention of the formation
to help patients with T2DM achieve better glycemic control, and accumulation of amyloid-β (Abeta) peptides into the
although conclusions from meta-analyses are mixed (81–84). neurotoxic oligomeric inclusions, both of which are considered
Eleven randomized, controlled trials that met the inclusion to be the AD trademarks. An aqueous extract of cinnamon
criteria were identified and enrolled 694 adults with T2DM both inhibits tau protein activity (a protein that becomes toxic
receiving and not receiving hypoglycemic medications. In 10 of when it accumulates and twists inside nerve cells in the
the studies, participants continued to take their hypoglycemic brain), and Abeta insult of neuronal cells in an in vitro model
medications during the cinnamon intervention period. The (100, 101). Indeed, cinnamon possesses neuroprotective
studies ranged from 4 to 16 weeks in duration, and 7 of effects by interfering with multiple oxidative stress and
the studies were double-blind. Cinnamon doses ranged from proinflammatory pathways. Additionally, cinnamon modulates
120 to 6000 mg/day. All 11 of the studies reported some endothelial functions and attenuates the vascular cell adhesion
reductions in FPG during the cinnamon intervention, and of molecules. Cinnamon polyphenols may induce AD epigenetic
the studies measuring hemoglobin A1c (HbA1c), very modest modifications. Cinnamon, particularly cinnamaldehyde, seems
decreases were also apparent with cinnamon, whereas changes to be effective and safe approaches for treatment and prevention
in the placebo groups were minimal. However, only four of AD onset and/or progression. However, further molecular
studies achieved the American Diabetes Association treatment and translational research studies as well as prolonged clinical
goals [FPG < 7.2 mmol/L (130 mg/dL) and/or HbAlc <7.0]. trials are required to establish the therapeutic safety and
It was concluded that cinnamon supplements added to standard efficacy in different Cinnamon spp.
Jiang: Journal of AOAC International Vol. 102, No. 2, 2019 399
Antioxidant effect.—Piperine, the active compound of black that BPB appears to have the potential to modulate perceived
pepper, has been demonstrated within in vitro studies to protect appetite by lowering ‘hunger,’ ‘desire to eat,’ and ‘prospective
against oxidative damage by inhibiting or quenching free consumption’ and increasing ‘satiety’ and ‘fullness’ without
radicals and reactive oxygen species. Both the oil and oleoresins affecting gastrointestinal wellbeing. Further experiments are
showed strong antioxidant activity in comparison with butylated needed to establish the relevant dose and mode of intake to
hydroxyanisole and butylated hydroxytoluene (143–145). Black optimize the effects.
pepper or piperine treatment has also been evidenced to lower Enhancing nutrient bioavailability.—Piperine has a passive
lipid peroxidation in vivo and beneficially influence cellular diffusion mechanism, high apparent permeability coefficient,
antioxidant status in a number of experimental situations of and short clearance time (165). It was suggested that piperine
oxidative stress (146, 147). promtes its efficient permeation through the epithelial barrier in
Anti-inflammatory effect.—Piperine has revealed remarkable the intestine (166). Piperine enhances the absorption of various
anti-inflammatory and analgesic activities (148). The anti- nutrients and drugs and functions as a bioavailability enhancer
inflammatory activity of piperine has been confirmed in of various substances such as coenzyme Q10, curcumin, and
many rat models (149). Both in vitro and in vivo rat models tea polyphenols (145). For example, when curcumin was
found that piperine inhibited 5-lipoxygenase and COX-2, two administrated with piperine at 20 mg/kg, its bioavailability
key enzymes involved in biosynthesis of proinflammatory increased by 154% in an animal study (167). Bioavailability
mediators that cause inflammation, pain and fever (150–152). enhancing of curcumin could be a preventive effect of piperine
Piperine also reduced the levels of proinflammatory cytokines on the intestinal and hepatic metabolism of curcumin (168).
such as IL-1β, IL-6, and TNF-α levels and inhibited activation Studies have shown that piperine remarkably increased the
of NF-κB within in vitro and in vivo animal studies (152–154). in vivo bioavailability of resveratrol by inhibiting its metabolism
In addition, piperine relieved pain in an arthritis animal model and decreasing the required dose of resveratrol in a clinical
(152, 155). Curcumin and piperine supplementation before and setting (169).
after exercise can attenuate some aspects of muscle damage (156). Mood and cognitive function.—Black pepper may exhibit
Antiallergic effect.—An animal model found that piperine antidepressant-like activity and have a cognition-enhancing
inhibited both histamine release and eosinophil infiltration effect via the regulation of neurotransmitter metabolism in
and also suppressed allergic airway inflammation and airway animals (170, 171).
hyperresponsiveness (157). Asthma is an inflammatory disease
caused by irregular immune responses in the airway mucosa. Turmeric
Piperine has shown deep inhibitory effects on airway inflammation
in a murine model of asthma from supressing type 2 helper T cells Bioactive components.—The major active constituents of
(Th2) cytokines (IL-4, IL-5, and IL-13), immunoglobulin E, turmeric are curcuminoids including curcumin (diferuloyl
eosinophil CCR3 expression, and by enhanced transforming methane), demethoxycurcumin, bisdemethoxycurcumin, and
growth factor–β (TGF-β) gene expression in the lungs. tetrahydrocurcumin. Curcumin is the active compound most
Therefore, it can be considered as a possible immunomodulator commonly studied using in vitro and in vivo (animal and human)
by downregulating Th2 cytokines (157). studies.
Digestion aid.—Black pepper may accelerate the overall Antioxidative and anti-inflammatory effects.—Curcumin
digestive process by enhancing the activity of digestive preparations in vitro have scavenged free radicals, inhibited
enzymes, increasing gastric acid and bile acid secretion, and lipid peroxidation and LDL, oxidation, and prevented
reducing food transit time (145). In animal studies, piperine was deoxyribonucleic acid (DNA) oxidative damage. Turmeric
found to enhance the activities of pancreatic amylase, lipase, also has exhibited powerful anti-inflammatory activity,
and chymotrypsin by 87, 37, and 30%, respectively, when possibly by inhibiting COX-2, prostaglandins, leukotrienes,
consumed through the diet (158). and other inflammatory mediators such as TNF-α, and NF-κB
Cardiovascular health.—Piperine has been shown to inhibit (2, 3). In a randomized controlled trial (172), it was shown that
lipid droplet accumulation in mouse macrophages that are curcumin supplementation (daily dose of 1 g/day) over 8 weeks
converted to foam cells in an animal study, suggesting it may significantly decreased serum concentrations of proinflammatory
help retard the progression in which fatty deposits build up in cytokines in 59 subjects with a metabolic syndrome. There
the arterial wall (159). Piperine also reduced plasma lipid and were significant reductions in serum concentrations of TNF-α,
lipoprotein levels in rats (160), inhibited platelet-derived growth IL-6, TGF-β, and MCP-1 following curcumin supplementation
factor-BB-induced proliferation and migration of vascular (P < 0.001).
smooth muscle cells in blood vessels (161), and lowered blood Cardiovascular health.—A number of laboratory, animal,
pressure in animals (162). More research is necessary to verify and human studies suggest that curcumin may have protective
the cardiovascular benefits of black pepper. effects on cardiac function, vascular health, and lipid profiles
Weight management.—Piperine may enhance energy (173, 174). In an uncontrolled study, 10 healthy human
expenditure or thermogenesis through the sympathetic nervous volunteers who received a dose of 500 mg curcumin per day
system by increasing levels of catecholamine and activating for 7 days had a 12% decrease in total serum cholesterol
the adrenal sympathetic nerves in animal studies (163). Zanzer levels and a 29% increase in HDL-C levels (175). Curcumin
et al. (164) recently examined the postprandial effect of a also reduced cholesterol levels in acute coronary syndrome
black pepper–based beverage (BPB) on glycaemia, appetite, patients in a clinical trial in which curcumin was administered
gastrointestinal well-being, gut hormones (peptide tyrosine– in various doses (45, 90, or 180 mg/day). It appeared that lower
tyrosine and GLP-1), and thyroid hormones postprandially after doses of curcumin were more effective than higher doses in this
a white wheat bread challenge in healthy adults, and concluded regard, in which 45 mg/day of curcumin reduced LDL and total
Jiang: Journal of AOAC International Vol. 102, No. 2, 2019 401
cholesterol levels with increased HDL concentrations (176). a population of community-dwelling older adults. A significant
In a 12 week randomized, double-blind, placebo-controlled trial time × treatment group interaction was observed for the
(177), subjects with T2D (n = 118), curcuminoid (1000 mg/day Montreal Cognitive Assessment (repeated-measures analysis;
plus piperine 10 mg/day) supplementation revealed significant time × treatment; F = 3.85, P < 0.05) in subjects who ingested
reductions in serum levels of total cholesterol, non–HDL-C 1500 mg/day Biocurcumax for 12 months. Subsequent analysis
and lipoprotein(a) with elevations in serum HDL-C levels in revealed that this association was driven by a decline in function
the curcuminoids group as compared with the placebo group. of the placebo group at 6 months that was not observed in the
Thus, curcuminoids supplementation could contribute to a curcumin treatment group. In addition, curcumin may have
reduced risk of cardiovascular events in dyslipidemic patients antidepressant effect. Chronic supplementation with curcumin
with T2D. Moreover, 12 weeks of curcumin (2000 mg/day (1000 mg/day) produced a significant antidepressant behavioral
Longvida®; Verdure Sciences) supplementation improved response in depressed patients by a reduction of 17 item
resistance of arterial endothelial function by increasing vascular Hamilton Depression Rating Scale and Montgomery-Asberg
NO bioavailability and reducing oxidative stress, while also Depression Rating Scale scores (195). Furthermore, curcumin
improving conduit artery endothelial function in healthy middle- decreases inflammatory cytokines IL-1β and TNF-α levela,
aged and older adults (178). In addition, curcumin can improve increases plasma brain-derived neurotrophic factor levels, and
metabolic profiles in patients with metabolic syndrome (179). decreases salivary cortisol concentrations
Gastrointestinal health.—A pilot trial examined the effect of Joint and muscle health.—The anti-inflammatory activity
standardized turmeric extract on symptoms of irritable bowel properties of curcumin may also help this bioactive compound
syndrome (a functional bowel disorder) in 207 otherwise maintain healthy joint function (196). In a well-described
healthy adults. Administrating a dose of either 72 or 144 mg animal model of rheumatoid arthritis, the arthritic index, a
turmeric extract for 8 weeks reduced the pain/discomfort score clinical measure of joint swelling, was used as the primary
significantly (22–25%), and approximately two-thirds of the end point for assessing the effect of turmeric extracts on
subjects reported an improvement in symptoms after treatment joint inflammation. The study showed turmeric extract
(180). A randomized, double-blind trial in patients with ulcerative containing 41% curcuminoids was effective in preventing joint
colitis suggested that consumption of 2 g/day curcumin reduced inflammation in rats (197). A number of human clinical trials
recurrence rates and improved the clinical activity index (181). have demonstrated that curcumin acts as an analgesic and anti-
In addition, in vitro and in vivo animal studies suggested that inflammatory agent for the management of arthritis (198, 199).
curcumin has anti-H. pylori activity and eradicated H. pylori Kuptniratsaikul et al. (200) found that patients with primary
from infected mice (182, 183). In a recent randomized trial knee OA who consumed a dose of 2 g/day turmeric extract for
(184), it was shown that an addition of curcumin (500 mg/day) 6 weeks had similar pain relief as the patients who consumed
on top of the standard antihelicobacter regimen in patients with 800 mg/day of ibuprofen (200). Haroyan et al. (201) compared
peptic ulcers is safe and improves dyspepsia symptoms but has the effects of CuraMed® (Terry Naturally) 500 mg capsules
no enhancing effect on the eradication of H. pylori infection. (333 mg curcuminoids) and Curamin® (Terry Naturally) 500 mg
Curcumin has been shown to be effective against development capsules (350 mg curcuminoids and 150 mg boswellic acid)
of hepatic steatosis and its progression to steatohepatitis (185, taken orally 3 times a day for 12 weeks in 201 patients with OA
186). In a randomized trial, an 8 week supplementation of in a three-arm, randomized, double-blinded, placebo-controlled
curcumin was associated with a significant reduction in liver trial. They found that curcumin complex reduced pain-related
fat content (78.9% improvement in the curcumin versus 27.5% symptoms in patients with OA, and curcumin in combination
improvement in the placebo group) in patients with nonalcoholic with boswellic acid is more effective, presumably because of the
fatty liver disease (NAFLD; 186). There were also significant synergistic effects of curcumin and boswellic acid.
reductions in BMI and serum levels of total cholesterol, LDL-C, Blood glucose control.—In vitro and in vivo animal studies
triglycerides, liver enzymes, and uric acid when compared with have found that curcumin lowered blood glucose levels
the placebo group (185, 186). through the suppression of glucose in the liver (202), reversed
Brain health and cognitive function.—Preventing the insulin resistance in fat cell cultures (203), increased glucose
accumulation of Abeta aggregation is an important factor uptake into skeletal muscle (204), and stimulated pancreatic
in maintaining healthy brain function. The accumulation of beta-cell function (205). Turmeric supplementation has
Abeta occurring in the brain is one of the leading causes of been shown to improve glucose indexes. A randomized
neurodegeneration (187). Curcumin enhanced Abeta clearance clinical trial, in which patients with T2DM were given
and reducedAbeta and plaque burdens in animal studies (188, 189). two 300 mg doses of curcuminoids daily for 8 weeks,
Animal studies with curcumin also found that this bioactive found that curcumin had a favorable effect on endothelial
ingredient has improved memory retention and prevented dysfunction in association with reductions of inflammation
oxidative damage (190, 191). In addition, a mouse study and oxidative stress in a similar manner to those randomized
showed that curcumin protected against the development of brain to the prescription medication group (atorvastatin; 206). In a
blood vessel spasm and limited secondary brain tissue death recent clinical trial, 46 patients with NAFLD were given 3 g
as a result of an inadequate blood supply (192). A population- turmeric in capsules each day for 12 weeks, and it was found
based cohort study in Singapore involving over 1000 mentally that turmeric consumption decreased serum levels of glucose,
competent Asian subjects aged 60–93 years showed that regular insulin, and HOMA-IR (207).
turmeric consumption helped preserve cognitive function even Weight management.—In cell cultures and an animal model
when low-to-moderate curry levels were consumed (193). for obesity, curcumin inhibited the formation of new blood
More recently, Rainey-Smith et al. (194) investigated the vessels (angiogenesis), decreased the transformation of young
ability of a curcumin formulation to prevent cognitive decline in fat cells into mature fat cells (adipogenesis), and reduced the
402 Jiang: Journal of AOAC International Vol. 102, No. 2, 2019
buildup of fat in the mature cells, which has implications for extract also plays a role in its ability to moderate the metabolism
lowering body fat and body weight gain in mice. Therefore, of glucose in the digestive tract (220). Specifically, a soluble fiber
curcumin may have a potential benefit in weight control. In a in fenugreek, galactomannan, becomes viscous and thickens the
human study on 40 subjects who had a weight loss <2% after intestinal contents, helping to maintain healthy glucose absorption
30 days of diet and intervention lifestyle, curcumin (221). In a human study, when fenugreek was incorporated into
administration for an additional 30 days increased weight loss food, it reduced the glycemic index (GI) by 21% compared with
from 1.88 to 4.91%, enhanced body fat reduction percentage standard food not treated with fenugreek (222). Furthermore, a
from 0.70 to 8.43%, and enhanced BMI reduction from 2.10 recent randomized, controlled crossover trial in healthy human
to 6.43% (208). Supplementation with curcumin (phytosomal subjects documented that replacing 10% of refined wheat flour
form; 1000 mg/day) was associated with a reduction in BMI and with fenugreek seed powder significantly reduced the glycemic
waist circumference in patients diagnosed with NAFLD (209). response and the GI of buns and flatbreads (223). It has been also
Chemoprevention.—Curcumin inhibited the proliferation of reported that fenugreek seeds at 10 g/day significantly decreased
various tumor cells in culture, prevented carcinogen-induced fasting blood glucose and HbA1c, serum levels of insulin,
cancers in rodents, and inhibited the growth of human tumors homeostatic model assessment for insulin resistance, and total
in various models (210). Numerous mechanisms for these cholesterol and triglycerides, and it increased serum levels of
outcomes have been implicated, and human data in this area adiponectin in type 2 diabetic patients (224).
are limited to a small number of study subjects. Large doses Satiety and weight management.—Because of its high fiber
of oral curcumin have biological activity in some patients with content, fenugreek could help promote satiety, which may
pancreatic cancer and marked tumor regression (73%) was potentially support weight management. Hydroxyisoleucine, a
observed in one subject (211). fenugreek extract, reduced body weight in obese mice (225).
In a single-blind, randomized, crossover study, 8 g fenugreek
Fenugreek fiber in a breakfast meal increased feelings of fullness and
reduced hunger, as well as reduced energy intake at lunch in
Bioactive components.—The chemical components 18 healthy obese subjects (226). Another small-scale, double-
of fenugreek seeds include a large carbohydrate fraction blind, randomized, placebo-controlled human trial showed
(mucilaginous fiber, galactomannan), steroidal saponins a consumption of 1200 mg fenugreek seed extract daily for
(e.g., diosgenin and trigogenin), free amino acids (e.g., 14 days significantly decreased fat consumption by 17%
hydroxyisoleucine and lysine), flavonoids. and alkaloids compared with a placebo in 12 healthy subjects (227).
(e.g., gentianine and trigonelline). Three important chemical Exercise and physical performance.—Prolonged exercise
constituents with functionality are steroidal sapogenins depletes muscle reserves of glycogen, which can place
(converted from saponin while passing through human intestinal limitations on physical performance. The speed of glycogen
tract), galactomannans, and 4-hydroxyisoleucine. resynthesis in muscle can, therefore, determine the rate of
Lipid metabolism and vascular health.—Several animal and recovery after exercise. A recent study in trained male cyclists
human studies have identified significant lipid-lowering activity documented that those who ingested a glucose beverage
with different fenugreek preparations (212–217). An animal with fenugreek extract (containing 2 mg/kg body weight of
study indicated that fenugreek fractions rich in steroid saponins 4-hydroxyisoleucine) right after high-intensity exercise had a
decreased total plasma cholesterol but did not change triglyceride 63% greater rate of muscle glycogen resynthesis than those
levels (212). The fiber content of fenugreek extract helped who consumed the glucose beverage without the fenugreek
moderate the metabolism of lipids in the digestive tracts of rats extract (228). However, in a subsequent study by the same
(213, 214). In a hamster model of diabetes, a fenugreek-active research group using a low-intensity exercise protocol, the
compound (4-hydroxyisoleucine) decreased elevated plasma fenugreek extract had no effects on glycogen resynthesis
triglyceride by 33% and total cholesterol levels by 22% (215). (229). Nevertheless, an animal study suggested fenugreek
Human data suggest that higher intakes may be required for extract may have beneficial effects on endurance capacity
lipid-lowing activity to become significant. An open label by increasing fatty acid use and sparing glycogen. An animal
clinical trial using a daily dose of 12.5–18 g seed powder in study found that mice that received a fenugreek extract
healthy volunteers demonstrated significant reductions in total (300 mg/kg) had increased exercise endurance compared with
cholesterol and LDL-C levels (216). Another clinical trial study those who did not (230).
also showed that serum levels of triglycerides and VLDL-C Liver health.—Animal studies suggest fenugreek may
were decreased significantly (30 and 30.6%, respectively) after help protect against liver changes induced by chronic alcohol
taking 10 grams/day powdered fenugreek seeds soaked in hot consumption. Administration of fenugreek seed extract to
water for 8 weeks in type 2 diabetic patients (217). Further alcohol-fed rats (200 mg/kg) reduced the levels of lipid
well-controlled, double-blind research is warranted, especially peroxidation products and protein carbonyl content, increased
to determine the optimum dosage levels. the activities of antioxidant enzymes, and restored the levels
Blood glucose metabolism.—Animal and in vitro studies have of thiol groups compared with the control (231). Animal
demonstrated that 4-hydroxyisoleucine, an amino acid extracted experiments have also found that fenugreek reduced the
from fenugreek seeds, is a key component in supporting triglyceride accumulation in the liver (232), a hallmark feature
glucose and lipid metabolism (218). Administrating fenugreek of hepatic steatosis, and regressed cholesterol gallstones
seed extract improved insulin signaling and sensitivity, which formation (233); both effects were accompanied by significant
promoted the cellular actions of insulin in fructose-fed animals. reductions in blood lipid levels.
This effect was comparable with that of metformin, a drug used Sexual health.—Fenugreek seed extract has demonstrated
to treat high blood sugar (219). The fiber content of fenugreek hormone modulatory activity, providing biological plausibility
Jiang: Journal of AOAC International Vol. 102, No. 2, 2019 403
for relieving menopausal symptoms. In a randomized, placebo- evidence that rosemary may promote brain health by inhibiting
controlled trial, treatment with fenugreek dehusked seed both acetylcholinesterase and butyrylcholinesterase in vitro,
extract at 600 mg/day resulted in a significant reduction which may help facilitate communication among cells in the
in menopausal symptoms; women aged 40–65 years in the brain (249, 250). A protective effect on dopaminergic neural
treatment group reported significantly less daytime hot cells (which involve behavior and cognition, mood, attention,
flashes and night sweats at 12 weeks (234). In addition to and learning) has been observed in a number of rosemary
improvements on various postmenopausal discomforts and constituents (251, 252). Furthermore, carnosic acid may
quality of life of women, there was a significant increase improve cell viability and blood flow to the brain, based on in
in plasma estradiol in the extract-treated group (235). vitro experiments (251, 253).
Moreover, Rao et al. (236) reported that fenugreek extract Vascular health.—Evidence suggests that rosemary extract
supplementation resulted in a significant increase in blood- could inhibit LDL-C oxidation in a biologically relevant human
free testosterone and E2 levels as well as sexual desire and cell culture system (254). Rosemary has shown antithrombotic
arousal, compared with the placebo. The results indicate that activity and may improve endothelial function both in vitro
fenugreek extract may be a useful treatment for increasing and in vivo (255, 256). At a 5% concentration, rosemary
sexual arousal and desire in women. significantly improved vascular function by inhibiting platelet
Recently, clinical studies also documented the effect of reactivity and arterial blood clot formation as well as enhancing
a specialized fenugreek seed extract (e.g., Testofen) on the flow-mediated vasodilation in animals (256). Further, rosemary
symptoms of possible androgen deficiency, sexual function, extract inhibited rabbit lung angiotensin I–converting enzyme
and serum androgen concentrations in healthy aging males (ACE) in vitro (257). This inhibition leads to less production
(237–240). Supplementation of the extract at a dose of of a chemical that causes arteries to constrict, suggesting that
600 mg/day for 12 weeks improved the Aging Male Symptom rosemary extract may have an antihypertensive effect. Clinical
questionnaire, a measure of possible androgen deficiency studies are needed to determine whether this effect is significant
symptoms; sexual function; and increased both total serum in humans.
testosterone and free testosterone in healthy middle-aged Blood glucose control.—In an animal model, a high dose of
and older men (237). Testofen demonstrated a significant rosemary extract (100 mg/kg or higher) significantly lowered
positive effect on physiological aspects of libido and may blood glucose levels and increased serum insulin concentrations
assist to maintain normal healthy testosterone levels (239). in diabetic rabbits compared with 50 mg/kg (258). Rosemary
A protodioscin-enriched fenugreek seed extract (500 mg/day) activated PPAR-γ, which plays an essential role in the regulation
increased serum-free testosterone levels up to 46% as well as of cellular functions and metabolism, leading to lower blood
sperm counts, and it improved mental alertness, mood, and levels of fatty acids and glucose (259). Furthermore, rosemary
libido in the male study population (238). is a potential inhibitor of alpha-glucosidase, which may help
reduce sugar absorption (260). Rosemary may also inhibit AGE
Rosemary formation in vitro (261), which suggests it has the potential
to protect against the development of diabetic complications.
Bioactive components.—Rosemary contains phenolic acids However, more studies are required in animals and humans to
and diterpenes including carnosic acid, carnosol, caffeic acid confirm this hypothesis.
and its derivatives (i.e., rosmarinic acid), flavonoids (apigenin, Skin care.—Destruction of collagen is a hallmark of skin
diosmin, luteolin), and tannins. Rosemary also contains volatile aging as a result of exposure to UV irradiation in which the
oils that consist of cineole, pinene, and camphor. matrix metalloproteinases (MMPs) play important roles
Antioxidant and anti-inflammatory effects.—Numerous in destructive processes. A water-soluble extract inhibited
laboratory tests indicate that rosemary has strong antioxidant UV-induced MMP-1 and showed potential benefits for
properties. Carnosic acid and carnosol likely account for preventing skin photodamage in vitro (262). Further, carnosic
over 90% of its antioxidant activity (241). Carnosic acid and acid has demonstrated photoprotective action on human skin
carnosol reduced membrane damage by 40–50% and inhibited cells exposed to UVA light in vitro. Rosemary extract inhibited
lipid peroxidation by 88–100 and 38–89%, respectively, oxidative damage to skin-surface lipids in both in vitro and in
under oxidative stress conditions in a cell culture testing. vivo studies (263). Rosemary may be a good candidate for an
Both compounds also lowered DNA damage induced by a antiskin aging agent, but more human data are needed.
dietary oxidant (242). Rosemary extract enhanced antioxidant Heptoprotective effects.—Rosemary extract has reduced
defenses and improved antioxidant status in aged rats (243). toxic chemical-induced liver damage and cirrhosis and has
Rosemary suppressed the activation of inflammatory improved detoxification systems in an animal model (264).
cytokines such as NF-κB and IL-1β and shut down specific Consumption of 200 mg/kg leaf extract can limit weight gain
enzymes (COX-2) involved in inflammation during in vitro induced by a high-fat diet and protect against obesity-related
experiments (244, 245). liver steatosis (build up of fat in the liver) in mice. However,
Cognition, mental health, and neuroprotection.— administrating a lower dose of the leaf extract at 20 mg/kg body
Inhalation of rosemary and lavender oils enhanced cognitive weight was ineffective for this purpose (265).
function in a randomized study of 140 subjects using a Chemopreventive and anticarcinogenic potential.—In vitro
cognitive assessment battery test and self-assessment mood studies suggest that rosemary extract may reduce the effects of
scale (246). The aroma of rosemary oil reduced test-taking carcinogenic or toxic agents in many human cell lines (266).
stress in graduate students (247). Rosemary extract had an One mechanism through which constituents in rosemary may
antidepressant-like effect through an interaction with the exert anticancer effects is by reducing the expression of a
monoaminergic system in a rat study (248). There is emerging number of proinflammatory genes (267).
404 Jiang: Journal of AOAC International Vol. 102, No. 2, 2019
References (25) Saito, M., & Yoneshiro, T. (2013) Curr. Opin. Lipidol. 24,
71–77. doi:10.1097/MOL.0b013e32835a4f40
(1) Tapsell, L.C., Hemphill, I., Cobiac, L., Patch, C.S., (26) Srinivasan, K. (2013) Food Funct. 4, 503–521. doi:10.1039/
Sullivan, D.R., French, M., Roodenrys, S., Keogh, J.B., c2fo30249g
Clifton, P.M., Williams, P.G., Fazio, V.A., & Inge, K.E. (2006) (27) Lee, C.Y., Kim, M., Yoon, S.W., & Lee, C.H. (2003) Phytother.
Med. J. Aust. 185, S4–24 Res. 17, 454–458. doi:10.1002/ptr.1172
(2) Kaefer, C.M., & Milner, J.A. (2008) J. Nutr. Biochem. 19, (28) Manjunatha, H., & Srinivasan, K. (2007) Can J. Physiol
347–361. doi:10.1016/j.jnutbio.2007.11.003 Pharmacol. 85(6):588-96
(3) Iriti, M., Vitalini, S., Fico, G., & Faoro, F. (2010) Molecules 15, (29) Raghavendra, R.H., & Naidu, K.A. (2009) Prostaglandins,
3517–3555. doi:10.3390/molecules15053517 Leukotrienes Essent. Fatty Acids 81, 73–78. doi:10.1016/j.
(4) Yashin, A., Yashin, Y., Xia, X., & Nemzer, B. (2017) plefa.2009.04.009
Antioxidants 6, 70. doi:10.3390/antiox6030070 (30) Guarini, G., Ohanyan, V.A., Kmetz, J.G., DelloStritto, D.J.,
(5) Srinivasan, K. (2005) Food Rev. Int. 21, 167–88. doi:10.1081/ Toppil, R.J., Thodeti, C.K., Meszaros, J.G., Dmron, D.S., &
FRI-200051872 Bratz, I.N. (2012) Am. J. Physiol. Heart Circ. Physiol. 303,
(6) Barnes, P.M., Bloom, B., & Nahin, R.L. (2007) Complementary H216–H223. doi:10.1152/ajpheart.00011.2012
and Alternative Medicine Use Among Adults and Children: (31) Ahuja, K.D., & Ball, M.J. (2006) Br. J. Nutr. 96, 239–242.
United States, 2007, National Health Statistics Reports; No. 12, doi:10.1079/BJN20061788
National Center for Health Statistics, Hyattsville, MD (32) Ahuja, K.D., Robertson, I.K., Geraghty, D.P., &
(7) Clarke, T.C., Black, L.I., Stussman, B.J., Barnes, P.M., & Ball, M.P. (2007) Eur J. Clin Nutr. 61, 326–333. doi:10.1038/
Nahin, R.L. (2015) Trends in the Use of Complementary Health sj.ejcn.1602517
Approaches Among Adults: United States, 2002–2012, National (33) Yuan, L.J., Qin, Y., Wang, L., Zeng, Y., Chang, H., Wang, J.,
Health Statistics Reports; No. 79, National Center for Health Wang, B., Wan, J., Chen, S.H., Zhang, Q.Y., Zhu, J.D.,
Statistics, Hyattsville, MD Zhou, Y., & Mi, M.T. (2016) Clin. Nutr. 35, 388–393.
(8) Su, D., & Li, L. (2011) J. Health Care Poor Underserved 22, doi:10.1016/j.clnu.2015.02.011
296–310. doi:10.1353/hpu.2011.0002 (34) Chaiyata, P., Puttadechakum, S., & Komindr, S. (2003) J. Med.
(9) Isbill, J., Kandiah, J., & Khubchandani, J. (2018) Health Assoc. Thai. 86, 854–860
Promot. Perspect. 8, 33–40. doi:10.15171/hpp.2018.04 (35) Ahuja, K.D., Robertson, I.K., Geraghty, D.P., &
(10) Opara, E.I., & Chohan, M. (2014) Int. J. Mol. Sci. 15, Ball, M.J. (2006) Am. J. Clin. Nutr. 84, 63–69. doi:10.1093/
19183–19202. doi:10.3390/ijms151019183 ajcn/84.1.63
(11) Neveu, V., Perez-Jiménez, J., Vos, F., Crespy, V., du Chaffaut, L. (36) Chaiyasit, K., Khovidhunkit, W., & Wittayalertpanya, S. (2009)
(2010) Database (Oxford) 2010, bap024. doi:10.1093/database/ J. Med. Assoc. Thai. 92, 108–113
bap024 (37) Islam, M.S., & Choi, H. (2008) Phytother. Res. 22(8):1025–1029.
(12) Craig, W.J. (1999) Am. J. Clin. Nutr. 70, 491–499. doi:10.1093/ doi:10.1002/ptr.2417
ajcn/70.3.491s (38) Kwon, D.Y., Hong, S.M., Ahn, I.S., Kim, Y.S., Shin, D.W., &
(13) Tuohy, K.M., Conterno, L., Gasperotti, M., & Viola, R. (2012) Park, S. (2009) Nutrition 25, 790–799. doi:10.1016/j.
J. Agric. Food Chem. 61, 8776–8782. doi:10.1021/jf2053959 nut.2008.12.006
(14) Etxeberria, U., Fernández-Quintela, A., Milagro, F.I., Aguirre, L., (39) Rau, O., Wurglics, M., Dingermann, T., Abdel-Tawab, M.,
Martínez, J.A., & Portillo, M.P. (2013) J. Agric. Food Chem. 61, Schubert-Zsilavecz, M. (2006) Pharmazie 61, 952–956
9517–9533. doi:10.1021/jf402506c (40) Zsombok, A. (2013) J. Diabetes Complications 27, 287–292.
(15) Lv, J., Qi, L., Yu, C., Yang, L., Guo, Y., Chen, Y., Bian, Z., doi:10.1016/j.jdiacomp.2012.11.006
Sun, D., Du, J., Ge, P., Tang, Z., Hou, W., Li, Y., Chen, J., (41) Yoshioka, M., St-Pierre, S., Suzuki, M., & Tremblay, A. (1998)
Chen, Z., & Li, L. (2015) BMJ. 351, h3942. doi:10.1136/bmj. Br. J. Nutr. 80, 503–510. doi:10.1017/S0007114598001597
h3942 (42) Westerterp-Plantenga, M.S., Smeets, A., & Lejeune, M.P. (2005)
(16) Chopan, M., & Littenberg, B. (2017) PLoS ONE 12, e0169876. Int. J. Obes. (Lond.) 29, 682–688. doi:10.1038/sj.ijo.0802862
doi:10.1371/journal.pone.0169876 (43) Janssens, P.L., Hursel, R., & Westerterp-Plantenga, M.S. (2014)
(17) Chen, Y.H., Zou, X.N., Zheng, T.Z., Zhou, Q., Qiu, H., Chen, Y.L., Appetite 77, 44–49. doi:10.1016/j.appet.2014.02.018
He, M., Du, J., Lei, H.K., & Zhao, P. (2017) Chin. Med. J. (44) Zhang, L.L., Liu, D.Y., Ma, L.Q., Luo, Z.D., Cao, T.B., Zhong, J.,
(Engl.) 130, 2241–2250. doi:10.4103/0366-6999.213968 Yan, Z.C., Wang, L.J., Zhao, Z.G., Zhu, S.J., Schrader, M.,
(18) Li, Q., Cui, Y., Jin, R., Lang, H., Yu, H., Sun, F., He, C., Thilo, F., Zhu, Z.M., & Tepel, M. (2007) Circ. Res. 100,
Ma, T., Li, Y., Zhou, X., Liu, D., Jia, H., Chen, X., & 1063–1070. doi:10.1161/01.RES.0000262653.84850.8b
Zhu, Z. (2017) Hypertension 70, 1291–1299. doi:10.1161/ (45) Diepvens, K., Westerterp, K.R., & Westerterp-Plantenga, M.S.
HYPERTENSIONAHA.117.09950 (2007) Am. J. Physiol. Regul. Integr. Comp. Physiol. 292,
(19) Anandakumar, P., Kamaraj, S., Jagan, S., Ramakrishnan, G., R77–R85. doi:10.1152/ajpregu.00832.2005
Vinodjkumar, R., & Devaki, T. (2008) Phytother. Res. 22, (46) Lejeune, M.P., Kovacs, E.M., & Westerterp-Plantenga, M.S.
529–533. doi:10.1002/ptr.2393 (2003) Br. J. Nutr. 90, 651–659. doi:10.1079/BJN2003938
(20) Manjunatha, H., & Srinivasan, K. (2007) Can. J. Physiol. (47) Hachiya, S., Kawabata, F., Ohnuki, K., Inoue, N., Yoneda, H.,
Pharmacol. 85, 588–596. doi:10.1139/y07-044 Yazawa, S., & Fushiki, T. (2007) Biosci. Biotechnol. Biochem.
(21) Spiller, F., Alves, M.K., Vieira, S.M., Carvalho, T.A., 71, 671–676. doi:10.1271/bbb.60359
Leite, C.E., Lunardelli, A., Poloni, J.A., Cunha, F.Q., & (48) Kawabata, F., Inoue, N., Yazawa, S., Kawada, T., Inoue, K., &
de Oliviera, J.R. (2008) J. Pharm. Pharmacol. 60, 473–478. Fushiki, T. (2006) Biosci. Biotechnol. Biochem. 70, 2824–2835.
doi:10.1211/jpp.60.4.0010 doi:10.1271/bbb.60206
(22) Kang, J.H., Kim, C.S., Han, I.S., Kwanda, T., & Yu, R. (2007) (49) Snitker, S., Fujishima, Y., Shen, H., Ott, S., Pi-Sunyer, X.,
FEBS Lett. 581, 4389–4396. doi:10.1016/j.febslet.2007.07.082 Furuhata, Y., Sato, H., & Takahashi, M. (2009) Am J. Clin. Nutr.
(23) Nilius, B., & Appendino, G. (2013) Rev. Physiol. Biochem. 89, 45–50. doi:10.3945/ajcn.2008.26561
Pharmacol. 164, 1–76. doi:10.1007/112_2013_11 (50) Janssens, P.L., Hursel, R., Martens, E.A., & Westerterp-
(24) Yang, S., Liu, L., Meng, L., & Hu, X. (2019) Chem.-Biol. Plantenga, M.S. (2013) PLoS One 8, e67786. doi:10.1371/
Interact. 297,1–7 journal.pone.0067786
406 Jiang: Journal of AOAC International Vol. 102, No. 2, 2019
(51) Yeoh, K.G., Kang, J.Y., Yap, I., Guan, R., Tan, C.C., We, A., & (78) Mollazadeh, H., & Hosseinzadeh, H. (2016) Iran J. Basic Med.
Teng, C.H. (1995) Dig. Dis. Sci. 40, 580–583 Sci. 19, 1258–1270. doi:10.22038/ijbms.2016.7906
(52) Mózsik, G., Szolcsányi, J., & Rácz, I. (2005) World J. (79) Gupta, J.S., Puri, S., Misra, A., Gulati, S., & Mani, K. (2017)
Gastroenterol. 11, 5180–5184. doi:10.3748/wjg.v11.i33.5180 Lipids Health Dis. 16, 113. doi:10.1186/s12944-017-0504-8
(53) Satyanarayana, M.N. (2006) Crit. Rev. Food Sci. Nutr. 46, (80) Akilen, R., Pimlott, Z., Tsiami, A., & Robinson, N. (2013)
275–328. doi:10.1080/1040-830491379236 Nutrition 29, 1192–1196. doi:10.1016/j.nut.2013.03.007
(54) Grossi, L., Cappello, G., & Marzio, L. (2006) (81) Costello, R.B., Dwyer, J.T., Saldanha, L., Bailey, R.L.,
Neurogastroenterol Motil. 18, 632–636. doi:10.1111/j.1365- Merkel, J., & Wambogo, E. (2016) J. Acad. Nutr. Diet 116,
2982.2006.00793.x 1794–1802. doi:10.1016/j.jand.2016.07.015
(55) Bergonzelli, G.E., Donnicola, D., Porta, N., & Corthésy- (82) Medagama, A.B. (2015) Nutr. J. 14, 108. doi:10.1186/s12937-
Theulaz, I.E. (2003) Antimicrob. Agents Chemother. 47, 015-0098-9
3240–3246. doi:10.1128/AAC.47.10.3240-3246.2003 (83) Allen, R.W., Schwartzman, E., Baker, W.L., Coleman, C.I., &
(56) Lai, P.K., & Roy, J. (2004) Curr. Med. Chem. 11, 1451–1460. Phung, O.J. (2013) Ann. Fam. Med. 5, 452–459. doi:10.1370/afm.1517
doi:10.2174/0929867043365107 (84) Qin, B., Polansky, M.M., & Sato, Y. (2009) J Nutr Biochem.
(57) Tremaroli, V., & Bäckhed, F. (2012) Nature 489, 242–249. 20(11):901-8
doi:10.1038/nature11552 (85) Anderson, R.A. (2008) Proc. Nutr. Soc. 67, 48–53. doi:10.1017/
(58) Turnbaugh, P.J., Ley, R.E., Mahowald, M.A., Magrini, V., S0029665108006010
Mardis, E.R., & Gordon, J.I. (2006) Nature 444, 1027–1031. (86) Zhu, R., Liu, H., Liu, C., Wang, L., Ma, R., Chen, B., Li, L.,
doi:10.1038/nature05414 Niu, J., Fu, M., Zhang, D., & Gao, S. (2017) Pharmacol. Res.
(59) Ley, R.E., Turnbaugh, P.J., Klein, S., & Gordon, J.I. (2006) 122, 78–89. doi:10.1016/j.phrs.2017.05.019
Nature 444, 1022–1026. doi:10.1038/4441022a (87) Camacho, S., Michlig, S., de Senarclens-Bezençon, C.,
(60) Karlsson, F.H., Tremaroli, V., Nookaew, I., Bergström, G., Meyalan, J., Pzzoli, M., Markram, H., & le Coutre, J. (2015)
Behre, C.J., Fagerberg, B., Nielsen, J., & Bäckhed., F. (2013) Sci. Rep. 5, 7919. doi:10.1038/srep07919
Nature 498, 99–103. doi:10.1038/nature12198 (88) Mang, B., Wolters, M., Schmitt, B., Klb, K., Lichtighagen, R.,
(61) Qin, N., Yang, F., Li, A., Prifti, E., Chen, Y., Shao, L., Guo, J., Stichtenoth, D.O., & Hahn, A. (2006) Eur. J. Clin. Invest. 36,
Le Chatelier, E., Yao, J., W, J., Zhou, J., Ni, S., Liu, L., Pons, N., 340–344. doi:10.1111/j.1365-2362.2006.01629.x
Batto, J.M., Kennedy, S.P., Leonard, P., Yuan, C., Ding, W., Chen, Y., (89) Hlebowicz, J., Darwiche, G., Björgell, O., & Almér, L.O. (2007)
Hu, Z., Zheng, B., Qian, G., Xu, W., Ehrlich, S.D., Zheng, S., & Am. J. Clin. Nutr. 85, 1552–1556. doi:10.1093/ajcn/85.6.1552
Li, L. (2014) Nature 513, 59–64. doi:10.1038/nature13568 (90) Solomon, T.P., & Blannin, A.K. (2007) Diabetes Obes. Metab.
(62) Karlsson, F.H., Fåk, F., Nookaew, I., Tremaroli, V., 9, 895–901. doi:10.1111/j.1463-1326.2006.00694.x
Fagerberg, B., Petranovic, D., Bäckhed, D., & Nielsen, J. (2012) (91) Solomon, T.P., & Blannin, A.K. (2009) Eur. J. Appl. Physiol.
Nat. Commun. 3, 1245. doi:10.1038/ncomms2266 105, 969–976. doi:10.1007/s00421-009-0986-9
(63) Kang, C., Zhang, Y., Zhu, X., Liu, K., Wang, X., Chen, M., (92) Hlebowicz, J., Hlebowicz, A., Lindstedt, S., Björgell, O.,
Wang, J., Chen, H., Hui, S., Huang, L., Zhang, Q., Zhu, J., Höglumd, P., Holst, J.J., Darwiche, G., & Almér, L.O. (2009)
Wang, B., & Mi, M. (2016) J. Clin. Endocrinol. Metab. 101, Am. J. Clin. Nutr. 89, 815–821. doi:10.3945/ajcn.2008.26807
4681–4689. doi:10.1210/jc.2016-2786 (93) Ziegenfuss, T.N., Hofheins, J.E., Mendel, R.W., Landis, J., &
(64) Hariri, M., & Ghiasvand, R. (2016) Adv. Exp. Med. Biol. 929, Anderson, R.A. (2006) J. Int. Soc. Sports. Nutr. 3, 45–53.
1–24. doi:10.1007/978-3-319-41342-6_1 doi:10.1186/1550-2783-3-2-45
(65) Fabio, A., Cermelli, C., Fabio, G, Nicoletti, P., & Quaglio, P. (94) Altschuler, J.A., Casella, S.J., MacKenzie, T.A., & Curtis, K.M.
(2007) Phytother. Res. 21, 374–377. doi:10.1002/ptr.1968 (2007) Diabetes Care 30, 813–816. doi:10.2337/dc06-1871
(66) Azumi, S., Tanimura, A., & Tanamoto, K. (1997) Biochem. (95) Blevins, S.M., Leyva, M.J., Brown, J., Wrigh, J.,
Biophys. Res. Commun. 234, 506–510. doi:10.1006/bbrc.1997.6668 Scofield, R.H. & Aston, C.E. (2007) Diabetes Care. 30,
(67) Rosti, L., & Gastaldi, G. (2005) Pediatrics 116, 1057. 2236–2237. doi:10.2337/dc07-0098
doi:10.1542/peds.2005-1521 (96) Suppapitiporn, S., Kanpaksi, N., & Suppapitiporn, S. (2006)
(68) Tabak, M., Armon, R., & Neeman, I. (1999) J. Ethnopharmacol. J. Med. Assoc. Thai. 89, S200–S205
67, 269–277. doi:10.1016/S0378-8741(99)00054-9 (97) Vanschoonbeek, K., Thomassen, B.J., Senden, J.M.,
(69) Cao, H., Urban, J.F., Jr, & Anderson, R.A. (2008) J. Nutr. 138, Wodzig, W.K.W.H., & van Loon, L.J.C. (2006) J. Nutr. 136,
833–840. doi:10.1093/jn/138.5.833 977–980. doi:10.1093/jn/136.4.977
(70) Kim, D.H., Kim, C.H., Kim, M.S., Kim, J.Y., Chung, J.H., (98) Moselhy, S.S., & Ali, H.K. (2009) Biol. Res. 42, 93–98.
Lee, J.W., Yu, B.P., & Chung, H.Y. (2007) Biogerontology 8, doi:/S0716-97602009000100009
545–554. doi:10.1007/s10522-007-9098-2 (99) Kanuri, G., Weber, S., Volynets, V., Spruss, A., Bischoff, S.C., &
(71) Roussel, A.M., Hininger, I., Benaraba, R., Ziegenfuss, T.N., & Bergheim, I. (2009) J. Nutr. 139, 482–487. doi:10.3945/jn.108.100495
Anderson, R.A. (2009) J. Am. Coll. Nutr. 28, 16–21 (100) Peterson, D.W., George, R.C., & Scaramozzino, F. (2009)
(72) Preuss, H.G., Echard, B., Polansky, M.M., & Anderson, R. J Alzheimers Dis. 17, 585–597. doi:10.3233/JAD-2009-1083
(2006) J. Am. Coll. Nutr. 25, 144–150 (101) Kim, D.S., Kim, J.Y., & Han, Y.S. (2007) J. Altern.
(73) Huang, J., Wang, S., Luo, X., Xie, Y., & Shi, X. (2007) Thromb. Complement. Med. 13, 333–340. doi:10.1089/acm.2006.6107
Res. 119, 337–342. doi:10.1016/j.thromres.2006.03.001 (102) Keating, A., & Chez, R.A. (2002) Altern. Ther. Health Med. 8,
(74) Qin, B., Dawson, H., Polansky, M.M., & Anderson, R.A. (2009) 89–91
Horm. Metab. Res. 41, 516–522 (103) Ozgoli, G., Goli, M., & Simbar, M. (2009) J. Altern.
(75) Tuzcu, Z., Orhan, C., Sahin, N., Juturu, V., & Sahin, K. (2017) Complement. Med. 15, 243–246. doi:10.1089/acm.2008.0406
Oxid. Med. Cell. Longevity 2017. doi:10.1155/2017/1583098 (104) Pongrojpaw, D., Somprasit, C., & Chanthasenanont, A. (2007)
(76) Byrne, A., Makadia, S., Sutherland, A., & Miller, M. J. Med. Assoc. Thai. 90, 1703–1709
(2017) Arch. Med. Res. 48, 483–487. doi:10.1016/j. (105) Smith, C., Crowther, C., Willson, K., Hotham, N., &
arcmed.2017.11.017 McMillian, V. (2004) Obstet. Gynecol. 103, 639–645.
(77) Maierean, S.M., Serban, M.C., Sahebkar, A., Ursoniu, S., doi:10.1097/01.AOG.0000118307.19798.ec
Serban, A., Penson, P., & Banach, M.; Lipid and Blood Pressure (106) Levine, M.E., Gillis, M.G., Koch, S.Y., Voss, A.C.,
Meta-alaysis Collaboration (LBPMC) Group (2017) J. Clin. Stern, R.M., & Koch, K.L. (2008) J. Altern. Complement. Med.
Lipidol. 11, 1393–1406. doi:10.1016/j.jacl.2017.08.004 14, 545–551. doi:10.1089/acm.2007.0817
Jiang: Journal of AOAC International Vol. 102, No. 2, 2019 407
(107) Bameshki, A., Namaiee, M.H., Jangjoo, A., Dadgarmoghaddam, M., (135) Arablou, T., Aryaeian, N., Valizadeh, M., Sharifi, F.,
Ghalibaf, M.H.E., Ghorbanzadeh, A., & Sheybani, S. (2018) Hosseini, A., & Djalali, M. (2014) Int. J. Food Sci. Nutr. 65,
Electron. Physician. 10, 6354–6362. doi:10.19082/6354 515–520. doi:10.3109/09637486.2014.880671
(108) Dabaghzadeh, F., Khalili, H., Dashti-Khavidaki, S., (136) Shidfar, F., Rajab, A., Rahideh, T., Khandouzi, N.,
Abbasian, L., Moeinifard, A. (2014) Expert Opin. Drug Saf. 13, Hosseini, S., & Shidfar., S. (2015) J. Complement. Integr. Med.
859–866, doi:10.1517/14740338.2014.914170 12, 165–170. doi:10.1515/jcim-2014-0021
(109) Zick, S.M., Ruffin, M.T., Lee, J., Normolle, D.P., Siden, R., (137) Mahluji, S., Attari, V.E., Mobasseri, M., Payahoo, L.,
Alrawi, S., & Brenner, D.E. (2009) Support Care Cancer 17, Ostadrahimi, A., & Golzari, S.E. (2013) Int. J. Food Sci. Nutr.
563–572. doi:10.1007/s00520-008-0528-8 64, 682–686. doi:10.3109/09637486.2013.775223
(110) Woo, H.M., Kang, J.H., Kawada, T., Yoo, H., Sung, M.K., & (138) Miyamoto, M., Matsuzaki, K., Katakura, M., Hara, T.,
Yu, R. (2007) Life Sci. 80, 926–931. doi:10.1016/j.lfs.2006.11.030 Tanabe, Y., & Shido, O. (2015) Int. J. Biometeorol. 59,
(111) Jung, H.W., Yoon, C.H., Park, K.M., Han, H.S., & Park, Y.K. 1461–1474. doi:10.1007/s00484-015-0957-2
(2009) Food Chem. Toxicol. 47, 1190–1197. doi:10.1016/j. (139) Mansour, M.S., Ni, Y.M., Roberts, A.L., Kelleman, M.,
fct.2009.02.012 Roychoudhury, A., & St-Onge, M.P. (2012) Metabolism 61,
(112) Dugasani, S., Pichika, M.R., Nadarajah, V.D., Balijepalli, M.K., 1347–1352. doi:10.1016/j.metabol.2012.03.016
Tandra, S., & Korlakunta, J.N. (2009) J. Ethnopharmacol. 127, (140) Ebrahimzadeh Attari, V., Ostadrahimi, A., Asghari Jafarabadi, M.,
515–520. doi:10.1016/j.jep.2009.10.004 Mehralizadeh, S., & Mahluki, S. (2016) Eur. J. Nutr. 55,
(113) Ahn, S.I., Lee, J.K., & Youn, H.S. (2009) Mol. Cells. 27, 2129–2136. doi:10.1007/s00394-015-1027-6
211–215. doi:10.1007/s10059-009-0026-y (141) Grzanna, R., Phan, P., Polotsky, A., Lindmark, L., &
(114) Sang, S., Hong, J., Wu, H., Liu, J., Yang, C.S., Pan, M.H., Fondoza, C.G. (2004) J. Altern. Complement. Med. 10,
Badamaev, V., & Ho, C.T. (2009) J. Agric. Food Chem. 57, 1009–1013. doi:10.1089/acm.2004.10.1009
10645–10650. doi:10.1021/jf9027443 (142) Kim, D.S., Kim, J.Y., & Han, Y.S. (2007) J Altern Complement
(115) Mozaffari-Khosravi, H., Naderi, Z., Dehghan, A., Med. 13(3):333-40
Nadjarzadeh, A., & Fallah Huseini, H. (2016) J. Nutr. Gerontol. (143) Kapoor, I.P., Singh, B., Singh, G., De Heuluani, C.S.,
Geriatr. 35, 209–218. doi:10.1080/21551197.2016.1206762 De Lampasona, M.P., & Catalan, C.A.N. (2009) J. Agric. Food
(116) Jiang, Y., Turgeon, D.K., Wright, B.D., Sidahmed, E., Chem. 57, 5358–5364. doi:10.1021/jf900642x
Ruffin, M.T., Brenner, D.E., Sen, A., & Zick, S.M. (2013) Eur. J. (144) Agbor, G.A., Vinson, J.A, Oben, J.E., & Ngogang, J.Y. (2007)
Cancer Prev. 22, 455–460. doi:10.1097/CEJ.0b013e32835c829b J. Herb. Pharmacother. 7, 49–64
(117) Nicoll, R., & Henein, M.Y. (2009) Int. J. Cardiol. 131, 408–409. (145) Srinivasan, K. (2007) Crit. Rev. Food Sci. Nutr. 47, 735–748.
doi:10.1016/j.ijcard.2007.07.107 doi:10.1080/10408390601062054
(118) Chrubasik, S., Pittler, M.H., & Roufogalis, B.D. (2005) (146) Kaleem, M., Sheema, K., Sarmad, H., & Bano, B. (2005)
Phytomedicine 12, 684–670. doi:10.1016/j.phymed.2004.07.009 Indian J. Physiol. Pharmacol. 49, 65–71
(119) Ghayur, M.N., Gilani, A.H., & Afridi, M.B. (2005) Vascul (147) Vijayakumar, R.S., & Nalini, N. (2006) Cell. Biochem. Funct.
Pharmacol. 43(4):234-41 24, 491–498. doi:10.1002/cbf.1331
(120) Alizadeh-Navaei, R., Roozbeh, F., Saravi, M., Pouramir, M., (148) Tasleem, F., Azhar, I., Ali, S.N., Perveen, S., & Mahmood, Z.A.
Jalali, F., & Moghadamnia, A.A. (2008) Saudi Med. J. 29, 1280–1284 (2014) Asian Pac. J. Trop. Dis. 7, S461–S468. doi:10.1016/
(121) Bordia, A., Verma, S.K., & Srivastava, K.C. (1997) S1995-7645(14)60275-3
Prostaglandins, Leukotrienes Essent. Fatty Acids 56, 379–384. (149) Mujumdar, A.M., Dhuley, J.N., Deshmukh, V.K., Raman, P.H., &
doi:10.1016/S0952-3278(97)90587-1 Naik, S.R. (1990) Jpn. J. Med. Sci. Biol. 43, 95–100
(122) Lumb, A.B. (1994) Thromb. Haemost. 71, 110–111 (150) Prasad, N.S., Raghavendra, R., Lokesh, B.R., & Naidu, K.A.
(123) Young, H.Y., Liao, J.C., Chang, Y.S., Luo, Y.L., Lu, M.S., & Peng, W.H. (2004) Prostaglandins, Leukotrienes Essent. Fatty Acids 70,
(2006) Am. J. Chin. Med. 34, 545–551. doi:10.1142/S0192415X06004089 521–528. doi:10.1016/j.plefa.2003.11.006
(124) Han, L.K., Morimoto, C., Zheng, Y.N., Li, W., Asami, E., (151) Stohr, J.R., Xiao, P.G., & Bauer, R. (2001) J Ethnopharmacol
Okuda, H., & Saito, M. (2008) Yakugaku Zasshi. 128, 1195–1201. 75, 133–139. doi:10.1016/S0378-8741(00)00397-4
doi:10.1248/yakushi.128.1195 (152) Bang, J.S., Ohda, H., Choi, H.M., Sur, B.J., Lim, S.J.,
(125) Fouda, A.M., & Berika, M.Y. (2009) Basic Clin. Pharmacol. Kim, J.Y., Yang, H.I., Yoo, M.C., Hahm, D.H., & Kim, K.S.
Toxicol. 104, 262–271. doi:10.1111/j.1742-7843.2008.00363.x (2009) Arthritis Res. Ther. 11, R49. doi:10.1186/ar2662
(126) Funk, J.L., Frye, J.B., Oyarzo, J.N., & Timmermann, B.N. (153) Kumar, S., Singhal, V., Roshan, R., Sharma, A.,
(2009) J. Nat. Prod. 27, 403–407. doi:10.1021/np8006183 Rembhotkar, G.W., & Ghosh, B. (2007) Eur. J. Pharmacol.
(127) Black, C.D., Herring, M.P., Hurley, D.J., & O’Connor, P. (2010) 575, 177–186. doi:10.1016/j.ejphar.2007.07.056
J. Pain 11, 894–903 (154) Pradeep, C.R., & Kuttan, G. (2004) Int. Immunopharmacol. 4,
(128) Matsumura, M.D., Zavorsky, G.S., & Smoliga, J.M. (2015) 1795–1803. doi:10.1016/j.intimp.2004.08.005
Phytother. Res. 29, 887–893. doi:10.1002/ptr.5328 (155) Bae, G.S., Kim, M.S., Jung, W.S., Seo, S.W., Yun, S.W., Kin, S.G.,
(129) Saraswat, M., Reddy, P.Y., Muthenna, P., & Reddy, G.B. (2009) Park, R.K., Kim, E.C., Song, H.J., & Park, S.J. (2010) Eur. J.
Br. J. Nutr. 101, 1714–1721. doi:10.1017/S0007114508116270 Pharmacol. 642, 154–162. doi:10.1016/j.ejphar.2010.05.026
(130) Dearlove, R.P., Greenspan, P., Hartle, D.K., Swanson, R.B., & (156) Delecroix, B., Abaïdia, A.E., Leduc, C., Dawson, B., &
Hargrove, J.L. (2008) J. Med. Food. 11, 275–281. doi:10.1089/ Dupont, G. (2017) J. Sports Sci. Med. 16, 147–153
jmf.2007.536 (157) Kim, S.H., & Lee, Y.C. (2009) J. Pharm. Pharmacol. 61,
(131) Al-Amin, Z.M., Thomson, M., Al-Qattan, K.K., 353–359. doi:10.1211/jpp/61.03.0010
Peltonen-Shalaby, R., & Ali, M. (2006) Br. J. Nutr. 96, (158) Platel, K., & Srinivasan, K. (2004) Indian J. Med. Res. 119,
660–666. doi:10.1079/BJN20061849 167–179
(132) Bhandari, U., Kanojia, R., & Pillai, K.K. (2005) (159) Matsuda, D., Ohte, S., Ohshiro, T., Jiang, W., Rudel, L.,
J. Ethnopharmacol. 97, 227–230. doi:10.1016/j.jep.2004.11.011 Hong, B., Si, S., & Tomoda, H. (2008) Biol. Pharm. Bull. 31,
(133) Nammi, S., Sreemantula, S., & Roufogalis, B.D. (2009) 1063–1066
Basic Clin. Pharmacol. Toxicol. 104, 366–373. doi:10.1111/ (160) Vijayakumar, R.S., & Nalini, N. (2006) J. Basic Clin. Physiol.
j.1742-7843.2008.00362.x Pharmacol. 17, 71–86
(134) Ojewole, J.A. (2006) Phytother. Res. 20, 764–772. doi:10.1002/ (161) Lee, K.P., Lee, K., Park, W.H., Kim, H., & Hong, H. (2015)
ptr.1952 J. Med. Food 18, 208–15. doi:10.1089/jmf.2014.3229
408 Jiang: Journal of AOAC International Vol. 102, No. 2, 2019
(162) Taqvi, S.I., Shah, A.J., & Gilani, A.H. (2008) J. Cardiovasc. (186) Rahmani, S., Asgary, S., Askar, G., Keshvari, M.,
Pharmacol. 52, 452–458. doi:10.1097/FJC.0b013e31818d07c0 Hataminpour, M., Feizi, A., & Sahebkar, A. (2016) Phytother.
(163) Westerterp-Plantenga, M., Diepvens, K., Joosen, A.M., Bérubé- Res. 30, 1540–1548. doi:10.1002/ptr.5659
Parent, S., & Tremblay, A. (2006) Physiol Behav. 89 85–91. (187) Gongadze, N., Antelava, N., & Kezeli, T. (2008) Georgian Med.
doi:10.1016/j.physbeh.2006.01.027 News. 155, 44–48
(164) Zanzer, Y.C., Plaza, M., Dougkas, A., Turner, C., & Östman, E. (188) Yang, F., Lim, G.P., Begum, A.N., Ubeda, O.J., Simmons, M.R.,
(2018) Food Funct. 9, 2774–2786. doi:10.1039/C7FO01715D Ambegaokar, S.S., Chen, P.P., Kayed, R., Glabe, C.G.,
(165) Khajuria, A., Zutshi, U., & Bedi, K. (1998) Ind. J. Exp. Biol. 36, Frautschy, S.A., & Cole, G.M. (2005) J. Biol. Chem. 280,
46–50 5892–5901. doi:10.1074/jbc.M404751200
(166) Khajuria, A., Thusu, N., & Zutshi, U. (2002) Phytomedicine 9, (189) Cashman, J.R., Ghirmai, S., Abel, K.J., & Fiala, M. (2008) BMC
224–231. doi:10.1078/0944-7113-00114 Neurosci. 9, S13. doi:10.1186/1471-2202-9-S2-S13
(167) Shoba, G., Joy, D., Joseph, T., Majeed, M., Rajendran, R., & (190) Ahmed, T., & Gilani, A.H. (2009) Pharmacol. Biochem. Behav.
Srinivas, P.S. (1998) Planta Med. 64, 353–356. 91, 554–559. doi:10.1016/j.pbb.2008.09.010
doi:10.1055/s-2006-957450 (191) Ishrat, T., Hoda, M.N., Khan, M.B., Yousuf, S., Ahmad, M.,
(168) Rinwa, P., & Kumar, A. (2012) Brain Res. 1488, 38–50. Khan, M.M., Ahmad, A., & Islam, F. (2009) Eur. Neuropsycho
doi:10.1016/j.brainres.2012.10.002 pharmacol. 19, 636–647. doi:10.1016/j.euroneuro.2009.02.002
(169) Johnson, J.J., Nihal, M., Siddiqui, I.A., Scarlett, C.O., (192) Wakade, C., King, M.D., Laird, M.D., Alleyne, C.H., Jr, &
Bailey, H.H., Mukhtar, H., & Ahmad, N. (2011) Mol. Nutr. Food Dhandapani, K.M. (2009) Antioxid. Redox. Signal. 11, 35–45.
Res. 55, 1169–1176. doi:10.1002/mnfr.201100117 doi:10.1089/ars.2008.2056
(170) Li, S., Wan, C., Wang, M., Li, W., Matsumoto, K., & Tang, Y. (193) Ng, T.P., Chiam, P.C., Lee, T., Chua, H.C., Lim, L., & Kua, E.H.
(2007) Life Sci. 80, 1373–1381. doi:10.1016/j.lfs.2006.12.027 (2006) Am. J. Epidemiol. 164, 898–906. doi:10.1093/aje/kwj267
(171) Wattanathorn, J., Chonpathompikunlert, P., Muchimapura, S., (194) Rainey-Smith, S.R., Brown, B.M., Sohrabi, H.R., Shah, T.,
Priprem, A., & Tankamnerdthai, O. (2008) Food Chem. Toxicol. Goozee, K.G., Gupta, V.B., & Martins, R.N. (2016) Br. J. Nutr.
46, 3106–3110. doi:10.1016/j.fct.2008.06.014 115, 2106–2113. doi:10.1017/S0007114516001203
(172) Panahi, Y., Hosseini, M.S., Khalili, N., Simental-Mendía, M., & (195) Yu, J.J., Pei, L.B., Zhang, Y., Wen, Z.Y., & Yang, J.L. (2015)
Sahebkar, A. (2016) Biomed. Pharmacother. 82, 578–582. J. Clin. Psychopharmacol. 35, 406–410. doi:10.1097/
doi:10.1016/j.biopha.2016.05.037 JCP.0000000000000352
(173) Srivastava, G., & Mehta, J.L. (2009) J. Cardiovasc. Pharmacol. (196) Park, C., Moon, D.O., Choi, I.W., Choi, B.T., Nam, T.J., Rhu, C.H.,
Ther. 14, 22–27. doi:10.1177/1074248408329608 Kwon, T.K., Lee, W.H., Kim, G.Y., & Choi, Y.H. (2007) Int. J.
(174) Fang, X.D., Yang, F., Zhu, L., Shen, Y.L., Wang, L.L., & Mol. Med. 20, 365–372. doi:10.3892/ijmm.20.3.365
Cheng, Y.Y. (2009) Clin. Exp. Pharmacol. Physiol. 36, 1177–1182 (197) Funk, J.L., Oyarzo, J.N., Frye, J.B., Chen, G., Lantz, R.C.,
(175) Soni, K.B., & Kuttan, R. (1992) Indian J. Physiol. Pharmacol. Sólyom, A.M., & Timmermann, B.N. (2006) J. Nat. Prod. 69,
36, 273–275 351–355. doi:10.1021/np050327j
(176) Alwi, I., Santoso, T., Suyono, S., Sutrisna, B., Suyatna, F.D., (198) Panahi, Y., Alishiri, G.H., Parvin, S., & Sahebkar, A. (2016) J.
Kresno, S.B., & Ernie, S. (2008) Acta Med. Indones. 40, 201–210 Diet Suppl. 13, 209–220. doi:10.3109/19390211.2015.1008611
(177) Panahi, Y., Khalili, N., Sahebi, E., Namazi, S., Reiner, Ž., (199) Amalraj, A., Varma, K., Jacob, J., Divya, C.,
Majeed, M., & Sahebkar, A. (2017) Complement. Ther. Med. 33, Kunnumakkara, A.B., Stohs, S.J., & Gopi, S. (2017) J. Med.
1–5. doi:10.1016/j.ctim.2017.05.006 Food. 20, 1022–1030. doi:10.1089/jmf.2017.3930
(178) Santos-Parker, J.R., Strahler, T.R., Bassett, C.J., Bispham, N.Z., (200) Kuptniratsaikul, V., Thanakhumtorn, S., Chinswangwantanakul, P.,
Chonchol, M.B., & Seals, D.R. (2017) Aging (Albany NY) 9, Wattanamongkonsil, L., & Thamlikitkul, V. (2009) J. Altern.
187–208. doi:10.18632/aging.101149 Complement. Med. 15, 891–897. doi:10.1089/acm.2008.0186
(179) Panahi, Y., Hosseini, M.S., Khalili, N., Naimi, E., Soflaei, S.S., (201) Haroyan, A., Mukuchyan, V., Mkrtchyan, N., Minasyan, N.,
Majed, M., & Sahebkar, A. (2016) Nutrition 32(10):1116–1122. Gasparyan, S., Sargsyan, A., Narimanyan, M., &
doi:10.1016/j.nut.2016.03.018 Hovhannisyan, A. (2018) BMC Complement. Altern. Med. 18, 7
(180) Bundy, R., Walker, A.F., Middleton, R.W., & Booth, J. (2004) (202) Kim, T., Davis, J., Zhang, A.J., He, X., & Matthews, S.T. (2009)
J. Altern. Complement. Med. 10, 1015–1018. doi:10.1089/ Biochem. Biophys. Res. Commun. 388, 377–382. doi:10.1016/j.
acm.2004.10.1015 bbrc.2009.08.018
(181) Hanai, H., Lida, T., Takeuchi, K., Wanatabe, F., Maruyama, Y., (203) Wang, S.L., Li, Y., Wen, Y., Chen, Y.F., Na, L.X., Li, S.T., &
Andoh, A., Tsujikawa, T., Kuujiyama, Y., Mitsuyama, K., Sun, C.H. (2009) Biomed. Environ. Sci. 22, 32–9. doi:10.1016/
Sata, M., Yamada, M., Iwaoka, Y., Kanke, K., Hirashi, H., S0895-3988(09)60019-2
Hirayama, K., Arai, H., Yoshii, S., Uchijima, M., Nagata, T., & (204) Best, L., Elliott, A.C., & Brown, P.D. (2007) Biochem.
Koide, Y. (2006) Clin. Gastroenterol. Hepatol. 4, 1502–1506. Pharmacol. 73, 1768–1775. doi:10.1016/j.bcp.2007.02.006
doi:10.1016/j.cgh.2006.08.008 (205) Cheng, T.C., Lin, C.S., Hsu, C.C., Chen, L.J., Cheng, K.C., &
(182) De, R., Kundu, P., Swarnakar, S., Ramamurthy, T., Cheng, J.T. (2009) Neurosci. Lett. 465, 238–241. doi:10.1016/j.
Chowdhury, A., Nair, G.B., & Mukhopadhyay, A.K. (2009) neulet.2009.09.012
Antimicrob. Agents Chemother. 53, 1592–1597. doi:10.1128/ (206) Usharani, P., Mateen, A.A., Naidu, M.U., Raju, Y.S., &
AAC.01242-08 Chandra, N. (2008) Drugs R. D. 9, 243–250
(183) Zaidi, S.F., Yamada, K., Kadowaki, M., Usmanghani, K., & (207) Navekar, R., Rafraf, M., Ghaffari, A., Asghari-Jafarabadi, M., &
Sugiyama, T. (2009) J. Ethnopharmacol. 121, 286–291. Khoshbaten, M. (2017) J. Am. Coll. Nutr. 36, 261–267. doi:10.1
doi:10.1016/j.jep.2008.11.001 080/07315724.2016.1267597
(184) Khonche, A., Biglaria, O., Panahi, Y., Valizadegan, G., Soflaei, S.S., (208) Di Pierro, F., Bressan, A., Ranaldi, D., Rapacioli, G.,
Ghamarchehreh, M.E., Majeed, M., & Sahebkar, A. (2016) Drug Giacomelli, L., & Bertucciloli, A. (2015) Eur. Rev. Med.
Res. (Stuttg.) 66, 444–448. doi:10.1055/s-0042-109394 Pharmacol. Sci. 19, 4195–4202
(185) Panahi, Y., Kianpour, P., Mohtashami, R., Jafari, R., (209) Panahi, Y., Kianpour, P., Mohtashami, R., Jafari, R., Simental-
Simental-Mendía, L.E., & Sahebkar, A. (2016) J. Cardiovasc. Mendía, L.E., & Sahebkar, A. (2017) Drug Res (Stuttg.) 67,
Pharmacol. 68, 223–229. doi:10.1097/FJC.0000000000000406 244–251. doi:10.1055/s-0043-100019
Jiang: Journal of AOAC International Vol. 102, No. 2, 2019 409
(210) Kunnumakkara, A.B., Anand, P., & Aggarwal, B.B. (2008) (236) Rao, A., Steels, E., Beccaria, G., Inder, W.J., & Vitetta, L.
Cancer Lett. 269, 199–225. doi:10.1016/j.canlet.2008.03.009 (2015) Phytother. Res. 29, 1123–1130. doi:10.1002/ptr.5355
(211) Dhillon, N., Aggarwal, B.B., Newman, R.A., Wolff, R.A., (237) Rao, A., Steels, E., Inder, W.J., Abraham, S., & Vitetta, L. (2016)
Kunnumakkara, A.B., Abbruzzese, J.L., Ng, C.S., Aging Male. 19, 134–142. doi:10.3109/13685538.2015.1135323
Badmaev, V., & Kurzrock, R. (2008) Clin Cancer Res. 14, (238) Maheshwari, A., Verma, N., Swaroop, A., Bagchi, M.,
4491–4499. doi:10.1158/1078-0432.CCR-08-0024 Preuss, H.G., Tiwari, K., & Bagchi, D. (2017) Int. J. Med. Sci.
(212) Petit, P.R., Sauvaire, Y.D., Hillaire-Buys, D.M., Leconte, O.M., 14, 58–66. doi:10.7150/ijms.17256
Baissac, Y.G., Ponsin, G.R., & Ribes, G.R. (1995) Steroids 60, (239) Steels, E., Ra, A., & Vitetta, L. (2011) Phytother. Res. 25,
674–680. doi:10.1016/0039-128X(95)00090-D 1294–1300. doi:10.1002/ptr.3360
(213) Boban, P.T., Nambisan, B., & Sudhakaran, P.R. (2006) Br. J. (240) Wilborn, C., Taylor, L., Poole, C., Foster, C., Willoughby, D., &
Nutr. 96, 1021–1029. https://doi.org/10.1017/BJN20061944 Kreider, R. (2010) Int. J. Sport Nutr. Exerc. Metab. 20, 457–465
(214) Srichamroen, A., Field, C.J., Thomson, A.B., & Basu, T.K. (2008) (241) Aruoma, O.I., Halliwell, B., & Aeschbach, R. (1992) Xenobiotica.
J. Clin. Biochem. Nutr. 43, 167–174. doi:10.3164/jcbn.2008060 22(2):257-68
(215) Narender, T., Puri, A., Shweta, A., Khaliq, T., Saxena, R., (242) Wijeratne, S.S.K., & Cuppett, S.L. (2007) J. Agric. Food Chem.
Bhatia, G., & Chandra, R. (2006) Bioorg. Med. Chem. Lett. 16, 55, 1193–1199. doi:10.1021/jf063089m
293–296. doi:10.1016/j.bmcl.2005.10.003 (243) Posadas, S.J., Caz, V., Largo, C., De la Gánadara, B.,
(216) Sowmya, P., & Rajyalakshmi, P. (1999) Plant Foods Hum. Nutr. Matallanas, B., Reglero, G., & De Miguel, E. (2009) Exp.
53, 359–365 Gerontol. 44, 383–389. doi:10.1016/j.exger.2009.02.015
(217) Chevassus, H., Gaillard, J.B., Farret, A., Costa, F., Gabillaud, I., (244) Huang, H.C., Huang, C.Y., Lin-Shiau, S.Y., & Lin, J.K. (2009)
Mas, E., Dupuy, A.M., Michel, F., Cantié, C., Renard, E., Mol. Carcinog. 48, 517–531. doi:10.1002/mc.20490
Galtier, F., & Petit, P. (2010) Eur. J. Clin. Pharmacol. 66, (245) Colica, C., Di Renzo, L., Aiello, V., De Lorenzo, A., &
449–55. doi:10.1007/s00228-009-0770-0 Abenavoli, L. (2018) Rev. Recent Clin. Trials 13, 240–242.
(218) Jetté, L., Harvey, L., Eugeni, K., & Lvens, N. (2009) Curr. doi:10.2174/157488711304180911095818
Opin. Investig. Drugs 10, 353–358 (246) Moss, M., Cook, J., Wesnes, K., & Duckett, P. (2003) Int. J.
(219) Kannappan., S., & Anuradha, C.V. (2009) Indian J. Med. Res. Neurosci. 113, 15–38
129, 401–408 (247) McCaffrey, R., Thomas, D.J., & Kinzelman, A.O. (2009) Holist.
(220) Hannan, J.M., Ali, L., Rokeya, B., Khaleque, J., Akhter, M., Nurs. Pract. 23, 88–93. doi:10.1097/HNP.0b013e3181a110aa
Flatt, P.R., & Abdl-Wahab, Y.H. (2007) Br. J. Nutr. 97, 514–521. (248) Machado, D.G., Bettio, L.E., & Cunha, M.P. (2009) Prog.
doi:10.1017/S0007114507657869 Neuropsychopharmacol. Biol. Psychiatry 33, 642–650.
(221) Srichamroen, A., Thomson, A.B., Field, C.J., & Basu, T.K. doi:10.1016/j.pnpbp.2009.03.004
(2009) Nutr Res. 29, 49–54. doi:10.1016/j.nutres.2008.11.002 (249) Adsersen, A., Gauguin, B., Gudiksen, L., & Jäger, A.K.
(222) Gopalpura, P.B., Jayanthi, C., & Dubey, S. (2007) Int. J. (2006) J. Ethnopharmacol. 104, 418–422. doi:10.1016/j.
Diabetes Dev. Ctries. 27, 4145 jep.2005.09.032
(223) Robert, S.D., Ismail, A.A., & Rosli, W.I. (2016) Eur. J. Nutr. 55, (250) Orhan, I., Aslan, S., Kartal, M., Sener, B., & Hüsnü Can
2275–2280. doi:10.1007/s00394-015-1037-4 Başer, K. (2008) Food Chem.108, 663–668. doi:10.1016/j.
(224) Rafraf, M., Malekiyan, M., Asghari-Jafarabadi, M., & foodchem.2007.11.023
Aliasgarzadeh, A. (2014) Int. J. Vitam. Nutr. Res. 84, 196–205. (251) Kim, S.J., Kim, J.S., Cho, H.S., Lee, H.J., Kim, S.Y., Kim, S.,
doi:10.1024/0300-9831/a000206 Lee, S.Y., & Chun, H.S. (2006) Neuroreport 17, 1729–1733.
(225) Handa, T., Yamaguchi, K., Sono, Y., & Yazawa, K. (2005) Biosci. doi:10.1097/01.wnr.0000239951.14954.10
Biotechnol. Biochem. 69, 1186–1188. doi:10.1271/bbb.69.1186 (252) Park, J.A., Kim, S., Lee, S.Y., Kim, C.s., Kim, D.K., Kim, S.J., &
(226) Mathern, J.R., Raatz, S.K., Thomas, W., & Slavin, J.L. (2009) Chun, H.S. (2008) Neuroreport 19, 1301–1304. doi:10.1097/
Phytother. Res. 23, 1543–1548. doi:10.1002/ptr.2795 WNR.0b013e32830abc1f
(227) Chevassus, H., Molinier, N., Costa, F., Gabillaud, I., (253) Satoh, T., Kosaka, K., Itoh, K., Kobayashi, A., Yamamoto, M.,
Mas, E., Dupuy, A.M., Michel, F., Cantié, C., Renard, E., Shimojo, Y., Kitajima, C., Cui, J., Kamins, J., Okamoto, S.,
Galtier, F., & Petit, P. (2010) Eur. J. Clin. Pharmacol. 66, Izumi, M., Shirasawa, T., & Lipton, S.A. (2008) J. Neurochem.
449–455. doi:10.1007/s00228-009-0770-0 104, 1116–1131. doi:10.1111/j.1471-4159.2007.05039.x
(228) Ruby, B.C., Gaskill, S.E., Slivka, D., & Harger, S.G. (2005) (254) Pearson, D.A., Frankel, E.N., Aeschbach, R., & German, J.B.
Amino Acids 28, 71–76. doi:10.1007/s00726-004-0143-z (1997) J. Agric. Food Chem. 45, 578–582. doi:10.1021/jf9603893
(229) Slivka, D., Cuddy, J., Hailes, W., Harger, S., & Ruby, B. (2008) (255) Lee, J.J., Jin, Y.R., Lee, J.H., Yu, J.Y., Han, X.H., Oh, K.W.,
Amino Acids 35, 439–444. doi:10.1007/s00726-007-0580-6 Hong, J.T., Kim, T.J., & Yun, Y.P. (2007) Planta Med. 73,
(230) Ikeuchi, M., Yamaguchi, K., Koyama, T., Sono, Y., & 121–127. doi:10.1055/s-2006-957066
Yazawa, K. (2006) J. Nutr. Sci. Vitaminol. (Tokyo) 52, 287–292. (256) Naemura, A., Ura, M., Yamashita, T., Arai, R., &
doi:10.3177/jnsv.52.287 Yamamoto, J. (2008) Thromb. Res. 122, 517–522. doi:10.1016/j.
(231) Kaviarasan, S., Sundarapandiyan, R., & Anuradha, C.V. (2008) thromres.2008.01.014
Cell Biol. Toxicol. 24, 391–400. doi:10.1007/s10565-007-9050-x (257) Kwon, Y.I., Vattem, D.A., & Shetty, K. (2006) Asia Pac. J. Clin.
(232) Reddy, R.L., & Srinivasan, K. (2009) Can. J. Physiol. Nutr. 15, 107–118
Pharmacol. 87, 684–693. doi:10.1139/y09-062 (258) Bakirel, T., Bakirel, U., Keleş, O.U., Ülgen, S.G., & Yardibi, H.
(233) Raju, J., & Bird, R.P. (2006) Int. J. Obes. (Lond.) 30, 1298– (2008) J. Ethnopharmacol. 116, 64–73. doi:10.1016/j.
1307. doi:10.1038/sj.ijo.0803254 jep.2007.10.039
(234) Steels, E., Steele, M.L., Harold, M., & Coulson, S. (2017) (259) Rau, O., Wurglics, M., Paulke, A., Zitzkowski, J.,
Phytother. Res. 31, 1316–1322. doi:10.1002/ptr.5856 Meindl, N., Bock, A., Dingermann, T., Abdel-Tawab, M., &
(235) Shamshad Begum, S., Jayalakshmi, H.K., Vidyavathi, H.G., Schubert-Zsilavecz, M. (2006) Planta Med. 72, 881–887.
Gopakumar, G., Abin, I., Balu, M., Geetha, K., Suresha, S.V., doi:10.1055/s-2006-946680
Vasundhara, M., & Krishnakumar, I.M. (2016) Phytother. Res. (260) Ercan, P., & El, S.N. (2018) Int. J. Biol. Macromol. 115,
30, 1775–1784. doi:10.1002/ptr.5680 933–939. doi:10.1016/j.ijbiomac.2018.04.139
410 Jiang: Journal of AOAC International Vol. 102, No. 2, 2019
(261) Hsieh, C.L., Peng, C.H., Chyau, C.C., Lin, Y.C., Wang, H.W., & (285) Szulińska, M., Kręgielska-Narożna, M., Świątek, J., Styś, P.,
Peng, R.Y. (2007) J Agric Food Chem. 55, 2884–2891. Kuźnar-Kamińska, B., Jakubowski, H., Walkowiak, J., &
doi:10.1021/jf0631833 Bogdański, P. (2018) Biomed. Pharmacother. 102, 792–797.
(262) Martin, R., Pierrard, C., Lejeune, F., Hilaire, P., Breton, L., & Bererd, F. doi:10.1016/j.biopha.2018.03
(2008) Eur. J. Dermatol. 18, 128–135. doi:10.1684/ejd.2008.0349 (286) Mahdavi-Roshan, M., Zahedmehr, A., Mohammad-Zadeh, A.,
(263) Calabrese, V., Scapagnini, G., Catalano, C., Dinotta, F., Sanati, H.R., Shakerian, F., Firouzi, A., Kiani, R., &
Geraci, D., & Morganti, P. (2000) Int. J. Tissue React. 22, 5–1 Nasrollahzadeh, J. (2013) Nutr. Health 22, 143–155.
(264) Galisteo, M., Suárez, A., Montilla, M.P., Torres, M.I., doi:10.1177/0260106014563446
Gil, A., & Navarro, M.C. (2006) Phytomedicine. 13, 101–108. (287) Rai, S.K., Sharma, M., & Tiwari, M. (2009) Life Sci. 85,
doi:10.1016/j.phymed.2004.06.024 211–219. doi:10.1016/j.lfs.2009.05.020
(265) Harach, T., Aprikian, O., Monnard, I., Moulin, J., Membrez, M., (288) Reinhart, K.M., Talati, R., White, C.M., & Coleman, C.I.
Bélor, J.C., Raab, T., Macé, K., & Darimont, C. (2009) Planta (2009) Nutr Res Rev. 22, 39–48. doi:10.1017/
Med. 76, 566–571. doi:10.1055/s-0029-1240612 S0954422409350003
(266) Cheung, S., & Tai, J. (2007) Oncol Rep. 17(6):1525-31 (289) Varshney, R., & Budoff, M.J. (2016) J. Nutr. 146, 416S–421S.
(267) Scheckel, K.A., Degner, S.C., & Romagnolo, D.F. (2008) doi:10.3945/jn.114.202333
J. Nutr. 138, 2098–2105. doi:10.3945/jn.108.090431 (290) Mahdavi-Roshan, M., Nasrollahzadeh, J.,
(268) Butt, M.S., Sultan, M.T., Butt, M.S., & Iqbal, J. Mohammad Zadeh, A., & Zahedmehr, A. (2016) Iran. Red
(2009) Crit. Rev. Food Sci. Nutr. 49, 538–551. Crescent Med. J. 18, e23871. doi:10.5812/ircmj.23871
doi:10.1080/10408390802145344 (291) Oboh, G., Ademiluyi, A.O., Agunloye, O.M., Ademosun, A.O., &
(269) Ban, J.O., Oh, J.H., Kim, T.M, Kim, D.J., Jeong, J.S., Ogunsakin, B.G. (2018) J. Diet. Suppl. 9, 1–14. doi:10.1080/19
Han, S.B., & Hong, J.T. (2009) Arthritis Res. Ther. 11, R145. 390211.2018.1438553
doi:10.1186/ar2819 (292) Al-Qattan, K.K., Thomson, M., Al-Mutawa’a, S., Al-Hajeri, D.,
(270) Keophiphath, M., Priem, F., Jacquemond-Collet, I., Drobiova, H., & Ali, M. (2006) J. Nutr. 136, 774S–776S.
Clément, K., & Lacasa, D. (2009) J. Nutr. 139, 2055–2060. doi:10.1093/jn/136.3.774S
doi:10.3945/jn.109.105452 (293) Lei, Y.P., Liu, C.T., Sheen, L.Y., Chen, H.W., & Lii, C.K.
(271) Salimzadeh, A., Alipoor, E., Dehghani, S., Yaseri, M., (2010) Mol. Nutr. Food Res. 54, S42–S52. doi:10.1002/
Hosseini, M., Feinle-Bisset, C., & Hosseinzadeh-Attar, M.J. mnfr.200900278
(2018) Int. J. Clin. Pract. 23, e13208. doi:10.1111/ijcp.13208 (294) Hosseini, M., Shafiee, S.M., & Baluchnejadmojarad, T.
(272) Blumenthal, M., Busse, W., & Goldberg, A. (1998) (2007) Pathophysiology 14, 109–112. doi:10.1016/j.
The Complete German Commission E Monographs: pathophys.2007.07.002
Therapeutic Guide to Herbal Medicine, Integrative Medicine (295) Benavides, G., Squadrito, G.L., Mills, R.W., Patel, H.D.,
Communications, Boston, MA Isbell, T.S., Patel, R.P., Darley-Usmar, V.M., Doeller, J.E., &
(273) Galeone, C., Tavani, A., Pelucchi, C., Negri, E., & Krauss, D.W. (2007) Proc. Natl. Acad. Sci. U S A 104,
La Vecchia, C. (2009) Eur. J. Nutr. 48, 120–123. doi:10.1007/ 17977–17982. doi:10.1073/pnas.0705710104
s00394-008-0771-2 (296) Reinhart, K.M., Coleman, C.I., Teevan, C., Vachhani, P., &
(274) Kwak, J.S., Kim, J.Y., Paek, J.E., Lee, Y.J., Kim, H.R., White, C.M. (2008) Ann. Pharmacother. 42, 1766–1771.
Park, D.S., & Kwon, O. (2014) Nutr Res Pract. 8, 644–654. doi:10.1345/aph.1L319
doi:10.4162/nrp.2014.8.6.644 (297) Rahman, K. (2007) Mol. Nutr. Food. Res. 51, 1335–1344.
(275) Budoff, M.J., Ahmadi, N., Gul, K.M., Liu, S.T., Flores, F.R., doi:10.1002/mnfr.200700058
Tiano, J., Takasu, J., Miller, E., & Tsimikas, M. (2009) Prev. (298) Steiner, M., & Li, W. (2001) J. Nutr. 131, 980S–984S.
Med. 49, 101–107. doi:10.1016/j.ypmed.2009.06.018 doi:10.1093/jn/131.3.980S
(276) Efendy, J.L., Simmons, D.L., Campbell, G.R., & (299) Fukao, H., Yoshida, H., Tazawa, Y., & Hada, T. (2007) Biosci.
Campbell, J.H. (1997) Atherosclerosis 132, 37–42. doi:10.1016/ Biotechnol. Biochem. 71, 84–90. doi:10.1271/bbb.60380
S0021-9150(97)00078-6 (300) Hiyasat, B., Sabha, D., Grotzinger, K., Kempfert, J.,
(277) Ferri, N., Yokoyama, K., Sadilek, M., Paoletti, R., Rauwalk, J.W., Mohr, F.W., & Dhein, S. (2009) Pharmacology
Apitz-Castro, R., Gelb, M.H., & Corsini, A. (2003) Br. J. 83, 197–204. doi:10.1159/000196811
Pharmacol. 138, 811–818. doi:10.1038/sj.bjp.0705126 (301) Pierre, S., Crosbie, L., & Duttaroy, A.K. (2005) Platelets 16,
(278) Durak, I., Oztürk, H.S., Olcay, E., & Güven, C. (2002) J. Herb. 469–473. doi:10.1080/09537100500129540
Pharmacother. 2, 19–32 (302) Scharbert, G., Kalb, M.L., Duris, M., Marschalek, C., &
(279) Lau, B.H.S. (2006) J. Nutr. 136, 765S–768S. doi:10.1093/ Kozek-Langenecker, S.A. (2007) Anesth. Analg. 105, 1214–
jn/136.3.765S 1218. doi:10.1213/01.ane.0000287253.92211.06
(280) Lei, Y.P., Chen, H.W., Sheen, L.Y., & Lii, C.K. (2008) J. Nutr. (303) Wojcikowski, K., Myers, S., & Brooks, L. (2007) Platelets 18,
138, 996–1003. doi:10.1093/jn/138.6.996 29–34. doi:10.1080/09537100600800636
(281) Gorinstein, S., Jastrzebski, Z., Namiesnik, J., Leontowicz, H., & (304) Womack, C.J., Lawton, D.J., Redmond, L., Todd, M.K., &
Trakhtenberg, S. (2007) Mol. Nutr. Food Res. 51, 1365–1381. Hargens, T.A. (2015) J. Int. Soc. Sports Nutr. 12, 23.
doi:10.1002/mnfr.200700064 doi:10.1186/s12970-015-0084-9
(282) Gonen, A., Harats, D., Rabinkov, A., Miron, T., Mirelman, D., (305) Drobiova, H., Thomson, M., Al-Qattan, K.,
Wilchek, M., Weiner, L., Ulman, E., Levkovitz, H., Peltonen-Shalaby, R., Al-Amin, Z., & Ali, M. (2011)
Ben-Shushan, D., & Shaish, A. (2005) Pathobiolog. 72, Evid. Based Complement. Alternat. Med. 2011, 703049.
325–334. doi:10.1159/000091330 doi:10.1093/ecam/nep011.
(283) Koscielny, J., Klüssendorf, D., Latza, R., Schmitt, R., (306) Jalal, R., Bagheri, S.M., Moghimi, A., & Rasuli, M.B.
Radtke, H., Siegel, G., & Kiesewetter, H. (1999) Atherosclerosis (2007) J. Clin. Biochem. Nutr. 41:218–223. doi:10.3164/
144, 237–249. doi:10.1016/S0021-9150(99)00060-X jcbn.2007031
(284) Williams, M.J., Sutherland, W.H., McCormick, M.P., (307) Liu, C.T., Wong, P.L., Lii, C.K., Hse, H., & Sheen, L.Y.
Yeoman, D.J., & de Jong, S.A. (2005) Phytother. Res. 19, (2006) Food Chem. Toxicol. 44, 1377–1384. doi:10.1016/j.
314–319. doi:10.1002/ptr.1663 fct.2005.07.013
Jiang: Journal of AOAC International Vol. 102, No. 2, 2019 411
(308) Thomson, M., Al-Qattan, K.K., Bordia, T., & Ali, M. (2006) ( 314) Borek, C. (2006) J. Nutr. 136, 810S–812S. doi:10.1093/jn/136.3.810S
J. Nutr. 136, 800S–802S doi:10.1093/jn/136.3.800S (315) Gupta, V.B., Indi, S.S., & Rao, K.S. (2009) Phytother. Res. 23,
(309) Liu, C.T., Hse, H., Lii, C.K., Chen, P.S., & Sheen, L.Y. 111–115. doi:10.1002/ptr.2574
(2005) Eur. J. Pharmacol. 516, 165–173. doi:10.1016/j. (316) Gupta, V.B., & Rao, K.S. (2007) Neurosci. Lett. 429, 75–80.
ejphar.2005.04.031 doi:10.1016/j.neulet.2007.09.042
(310) Sobenin, I.A., Nedosugova, L.V., Filatova, L.V., (317) Chauhan, N.B., & Sandoval, J. (2007) Phytother Res. 21,
Balabolkin, M.I., Gorchakova, T.V., & Orekhov, A.N. (2008) 629–640. doi:10.1002/ptr.2122
Acta Diabetol. 45, 1–6. doi:10.1007/s00592-007-0011-x (318) Salman, H., Bergman, M., Bessler, H., Punsky, I., &
(311) Wang, J., Zhang, X., Lan, H., & Wang, W. (2017) Food Nutr. Djaldetti, M. (1999) Int. J. Immunopharmacol. 21, 589–597.
Res. 61, 1377571. doi:10.1080/16546628.2017.1377571 doi:10.1016/S0192-0561(99)00038-7
(312) Aguilera, P., Chánez-Cárdenas, M.E., Ortiz-Plata, A., (319) Hassan, Z.M., Yaraee, R., Zare, N., Ghazanfari, T.,
Léon-Aparicio, D., Barrera, D., Espinoza-Rojo, M., Sarraf Nejad, A.H., & Nazori, B. (2003) Int. Immunopharmacol.
Villeda-Hernández, J., Sánchez-García, A., & 3, 1483–1489. doi:10.1016/S1567-5769(03)00161-9
Maldonado, P.D. (2010) Phytomedicine 17, 241–247. (320) Chandrashekar, P.M., & Venkatesh, Y.P. (2009) J.
doi:10.1016/j.phymed.2009.06.004 Ethnopharmacol. 124, 384–390. doi:10.1016/j.jep.2009.05.030
(313) Saleem, S., Ahmad, M., Ahmad, A.S., Yousuf, S., Asari, M.A., (321) Ishikawa, H., Saeki, T., Otani, T., Suzuki, T., Shimozuma, K.,
Khan, M.B., Ishrat, T., & Islam, F. (2006) J. Med. Food. 9, Nishino, H., Fakuda, S., & Morimoto, K. (2006) J. Nutr. 136,
537–544. doi:10.1089/jmf.2006.9.537 816S–820S. doi:10.1093/jn/136.3.816S