Journal of Traditional and Complementary Medicine Vo1. 2, No. 2, pp.

115-122
Copyright © 2011 Committee on Chinese Medicine and Pharmacy, Taiwan.

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Journal homepagĞŚƩƉ͗ͬͬǁǁǁ͘ũƚĐŵ͘Žƌg

Therapeutic Potential of Chinese Herbal Medicines

in Alcoholic Liver Disease

Kuan-Hung Lu, Chun-Ting Liu, Rajasekaran Raghu, and Lee-Yan Sheen*

Institute of Food Science and Technology, National Taiwan University, Taipei, Taiwan

Abstract
Alcoholic liver disease (ALD) is a complex chronic disease and is associated with a spectrum of liver injury ranging
from steatosis and steatohepatitis to fibrosis and cirrhosis. Since effective therapies for ALD are still limited, Chinese
herbal medicine is thought to be an important and alternative approach. This review focuses on the current scientific
evidence of ALD by ten Chinese Materia Medica (中藥 zhōng yào), including Salviae Miltiorrhizae Radix (丹參 dān
shēn), Notoginseng Radix (三七 sān qī), Lycii Fructus (枸杞子 gǒu qǐ zǐ), Cnidii Fructus (蛇床子 shé chuáng zǐ),
Gentianae Radix (龍膽 lóng dǎn), Puerariae Radix (葛根 gé gēn), Puerariae Flos (葛花 gé huā), Magnoliae Officinalis
Cortex (厚朴 hòu pò), Platycodonis Radix (桔梗 jié gěng), and Trigonellae Semen (胡蘆巴 hú lú bā). Potential
mechanisms of these herbal medicines in ALD are involved in amelioration of enhanced inflammation, reduction of
hepatic oxidative stress and lipogenesis, and enhancement of intestinal permeability in alcohol-induced liver injury
models in vitro and in vivo . Accordingly, the evidenced therapeutic potential suggests that these herbs are promising
candidates for prevention and development of new drugs for ALD in the future.

Key words: Alcoholic liver disease, Alcohol-induced liver injury, Herbal medicine, Chinese Materia Medica,
Traditional Chinese medicine

Introduction ALD is a complex chronic disease and typically

progresses through multiple stages of alcoholic steatosis,
World Health Organization has reported that the
hepatitis and cirrhosis to end-stage liver disease (Haber
harmful use of alcohol is one of the world’s leading
et al., 2003; Seth et al., 2008). The major feature of
health risks. Approximately 4.5% of the global burden
ALD is the enhanced inflammation in liver during
of diseases and injury can be attributable to alcohol,
alcohol exposure. Dysregulated cytokine metabolism
which results in approximately 2.5 million deaths each
and activity such as tumor necrosis factor (TNF-α) are
year (World Health Organization, 2011). Chronic or
crucial to the initiation of alcohol-induced liver injury
excessive alcohol consumption is one of the major
(An et al., 2012). In addition, hepatic oxidative stress
causes of liver disease and injury. Since the liver is the
is known to play a prime role in the pathogenesis of
largest human organ and metabolizes various substances
ALD (Bondy, 1992). Induction of cytochrome P450 2E1
that can damage the body, it is important to prevent
(CYP2E1) by alcohol is also another key pathway since
damage to healthy liver or repair the damaged liver from
the pathological changes in early alcoholic liver injuries
alcoholic liver disease (ALD) for a healthy life (Chien et
such as steatosis and steatohepatitis are associated
al., 2011).

*Correspondence to:
Dr. Lee-Yan Sheen. Institute of Food Science and Technology, National Taiwan University, No. 1, Sec. 4, Roosevelt Road, Taipei 10617, Taiwan,
TEL: +886-2-3366-4129, FAX: +886-2-2362-0849, E-mail: [email protected]


 Lu et al . / Journal of Traditional and Complementary Medicine 2 (2012) 115-122

with CYP2E1 levels ( Stewart et al., 2001; Wu and

Cederbaum, 2005). Moreover, alcohol can impair fat
oxidation and stimulate lipogenesis by interfering with
DNA binding and transcription-activating properties of
peroxisome proliferator-activated receptor-α (PPARα)
and activating sterol regulatory element-binding protein
1 (SREBP-1) (You et al., 2002; You and Crabb, 2004).
Understanding the mechanism underlying alcohol-
Figure 1. Structures of cryptotanshinone and tanshinone IIA from
induced effects provides an array of potential candidate
Salvia miltiorrhiza
for novel new therapeutic targets to reverse ALD.
In traditional Chinese medicine (TCM), liver disease
such as fibrosis is perceived to be caused by poor blood active hepatoprotective components. In primary rat
circulation, toxin accumulation, and energy deficiency. hepatocytes, 10 μM cryptotanshinone suppressed
Accordingly, Chinese medicine used therapy to treat alcohol-induced lipid accumulation, and inhibited
liver injury is mainly based on increasing blood activation and nuclear translocation of sterol regulatory
circulation, eliminating toxins, resolving stasis, and element-binding protein 1 (SREBP-1) and the
enhancing body immunity (Feng et al., 2009). However, consequent transactivation of the target genes involved
perspectives on evidence-based medicine nowadays are in fatty acid biosynthesis (Yin et al., 2009a). On the
encouraging medical practitioners to be guided in their other hand, 10 μM tanshinone IIA protected RAW 264.7
practice by available scientific evidence in terms of cells from alcohol-induced production of superoxide
efficacy and safety for individual therapies (Fogden and radical, activation of NADPH oxidase, and subsequently
Neuberger, 2003). In the present review, an attempt is death of the cells. Alcohol-induced expressions of
made to survey and comprehensively compile the recent CD14, iNOS, and SCD1 were completely reversed by
scientific evidence regarding Chinese Materia Medica tanshinone IIA. Also, tanshinone IIA effectively blocked
(CMM) (中藥 zhōng yào) and ALD through PubMed alcohol-induced fat accumulation in rat hepatoma
database (http://www.ncbi.nlm.nih.gov/pubmed/). All cells (H4IIEC3). Consequently, tanshinone IIA is the
CMMs shown in this review were selected due to their major active component of SMR to inhibit alcoholic
experimental evidences in vivo and/or in vitro . liver disease by reducing alcohol-induced Kupffer
cell sensitization, decreasing synthesis of reactive
Chinese herbal medicines against alcoholic oxygen/nitrogen species and fatty acid synthesis, and
liver disease stimulating fatty acid oxidation (Yin et al., 2008).

Notoginseng Radix (三七 sān qī; the root of Panax

Salviae Miltiorrhizae Radix (丹參 dān shēn; the root
notoginseng (Burk.) F.H. Chen, Araliaceae)
of Salvia miltiorrhiza , Labiatae)
Notoginseng Radix is known in TCM to improve
Salviae Miltiorrhizae Radix (SMR) has been used in
blood circulation and has been used to treat angina
the treatment of hypertension, coronary heart disease
pectoris due to its property to increase coronary blood
and myocardial infarction in TCM (Lei and Chiou,
flow. Bioactivities associated with Panax notoginseng
1986; Sun et al., 2005; Wang et al., 1989). Also, it has
include anti-inflammatory, analgesic, antitumor,
been used widely to treat chronic liver disease. An in
antihypertensive, anti-atherosclerotic, antithrombotic,
vivo study elucidated the protective effect of SMR
neuroprotective and hepatoprotective effects (Ng,
on chronic alcoholic liver injury employing a mice
2006; Pan et al., 2011). An animal study elucidated the
model (Xiong et al., 2005). Administration of SMR
hepatoprotective effects exerted by a hot water extract
(5 ml/kg bw, i.p.) could alleviate the alcohol-induced
of P. notoginseng (PNG) in alcohol-fed ICR mice (Lin et
fatty degeneration and adiponecrosis of hepatic cells
al., 2003). PNG (10 mg/kg bw, p.o.) prevented the rise
in Kunming mice. The protective mechanisms of SMR
in serum glutamate–oxaloacetate transaminase (sGOT,
were probably due to the down-regulation of TLR-4 and
AST) and glutamate–pyruvate transaminase (sGPT,
HO-1 mRNA expressions and significant decrease of
ALT), and inhibited the hepatic lipid peroxidation
TLR-4 positive cell number in the animal study.
(26% inhibition rate) against chronic alcohol-induced
Cryptotanshinone and tanshinone IIA (Figure 1),
hepatotoxicity.
diterpenes contained in SMR, were considered as


 Lu et al . / Journal of Traditional and Complementary Medicine 2 (2012) 115-122

studies showed that osthole (40 mg/kg bw, p.o. )

dramatically decreased lipid accumulation to inhibit
development of alcohol-induced fatty liver in Kunming
mice (Sun et al., 2009). The potential mechanisms
were related to reduction of hepatic oxidative stress,
enhancement of antioxidative enzyme activity, reduction
Figure 2. Structure of polysaccharide from Lycium barbarum of lipid accumulation and peroxidation, and regulation
the gene expressions of diacylglycerol acyltransferase
Lycii Fructus (枸杞子 gǒu qǐ zǐ; the fruit of Lycium (DGAT), 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA)
barbarum , Solanaceae) reductase and cholesterol 7α-hydroxylase (CYP7A)
Lycii Fructus, commercially known as goji berry, has mediated by increasing the peroxisome proliferator-
historically been used in TCM to improve eyesight and activated receptor-α (PPARα) mRNA expression (Sun et
to strengthen the liver and kidney (Lee et al., 2012). al., 2010; Zhang et al., 2011).
The bioactivity of Lycii Fructus is mainly attributed to
its polysaccharide complex (Figure 2), which consists Gentianae Radix (龍膽 lóng dǎn; the root of
of six monosaccharides (galactose, glucose, rhamnose, Gentiana manshurica Kitagawa, Gentianaceae)
arabinose, mannose, and xylose). A recent in vivo study Gentiana manshurica Kitagawa is abundantly
reported that Lycium barbarum polysaccharide (LBP) at distributed in northeastern China and has been used
a dose of 300 mg/kg bw significantly ameliorated liver traditionally as a folk remedy by Chinese people
injury by decreasing serum aspartate aminotransferase suffering from chronic liver disease (Wang et al.,
(AST) and alanine aminotransferase (ALT) activities 2010). A recent in vivo study showed the protective
and improving the antioxidant functions in alcohol- effects of Gentianae Radix methanolic extract (GM)
fed rats (Cheng and Kong, 2011). Moreover, LBP on acute alcohol-induced fatty liver (Lian et al., 2010).
prevented the progression of alcohol-induced fatty liver Treatment of GM (200 mg/kg bw) significantly reduced
by decreasing the levels of serum triglycerides, total the increases in serum aspartate aminotransferase
cholesterol, and low density lipoprotein cholesterol, and (AST) and alanine aminotransferase (ALT) levels, and
by increasing high density lipoprotein cholesterol level. the serum and hepatic triglyceride levels in ethanol-
administered C57BL/6 mice. GM was also found to
Cnidii Fructus (蛇床子 shé chuáng zǐ; the fruit of prevent alcohol-induced hepatic steatosis and necrosis
Cnidium monnieri (L.) Cusson, Apiaceae) by suppressing the elevation of malondialdehyde
Cnidii Fructus has been used in the treatment of skin (MDA) levels, restoring the glutathione (GSH) levels,
disease and gynecopathy in Chinese herbal medicine and enhancing the superoxide dismutase (SOD), catalase
for many years (Lian, 2003). Osthole (Figure 3) is (CAT), and glutathione peroxidase (GPx) activities.
a coumarin isolated from Cnidii Fructus. Modern Moreover, GM efficaciously abrogated cytochrome
pharmacological studies reported that osthole prevented P450 2E1 (CYP2E1) induction and significantly reduced
the development of hepatitis and hepatocellular the nuclear translocation of activating sterol regulatory
carcinoma induced by anti-Fas antibody in mice element-binding protein 1 (SREBP-1) in alcohol-treated
(Okamoto et al., 2003; Okamoto et al., 2005). Recent mice. In summary, GM possessed the ability to prevent
alcohol-induced acute liver steatosis by blocking
CYP2E1-mediated free radical scavenging effects and
SREBP-1-regulated fatty acid synthesis.

Puerariae Radix (葛根 gé gēn; the root of Puerariae

lobata , Leguminosae) and Puerariae Flos (葛花 gé
huā; the flower of P. lobata )
Puerariae Radix (PR) and Puerariae Flos (PF) have
been used in TCM to counteract problems associated
with alcohol drinking and liver injury since ancient
times (Keung and Vallee, 1998). The hepatoprotective
effects of PR and PF in alcoholic liver damage have
Figure 3. Structure of osthole from Cnidium monnieri been experimentally demonstrated in animal studies


 Lu et al . / Journal of Traditional and Complementary Medicine 2 (2012) 115-122

(Lee et al., 2001). Water extracts of PR and PF (mixed activity levels. The possible mechanism of tectoridin
with the diets based on 1.2 g of raw PR or PF/kg bw/ to inhibit alcohol-induced hepatotoxicity was mainly
day) were reported to normalize antioxidant enzymes, by modulating the disturbance of PPARα pathway and
including significant increase of the Cu/Zn superoxide ameliorating mitochondrial function.
dismutase (SOD) and/or catalase (CAT) activities and
Magnoliae Officinalis Cortex (厚朴 hòu pò; the
decrease of the glutathione peroxidase (GPx) activity,
stem bark of Magnolia officinalis Rehd. et Wols,
to the control level in the alcohol-treated Sprague-
Magnoliaceae)
Dawley rats. Similarly, another animal study showed
Magnoliae Officinalis Cortex (MOC) is a traditional
that PR water extract (mixed with the diets based on 1.5
Chinese herbal medicine that has been used for
g of raw PR/kg bw/day) alleviated the adverse effect of
treatment of gastrointestinal disorders, anxiety and
alcohol ingestion in Sprague-Dawley rats by enhancing
allergic disease (Lee et al., 2011). A recent study
the lipid metabolism as well as the hepatic antioxidant
showed that the ethanolic extract of MOC (50 μg/ml)
defense system (Lee, 2004). Moreover, a recent study
was able to protect alcohol-induced cell death by
showed that the inhibitory effect of PR extract (mixed
decreasing the production of TNF-α, reactive oxygen
with alcohol based on 3 g of raw PR/kg bw/day, p.o.) on
species and superoxide anion radicals, and by inhibiting
alcohol-induced liver damage in Wistar rats was through
the activation of NADPH in RAW264.7 cells. In
enhancement of intestinal permeability to improve
ethanol diet-fed animal model, Wistar rats treated
intestinal barrier dysfunction induced by alcohol (Zhang
with the ethanolic extract of MOC (45 mg/kg bw/day)
et al., 2009).
completely reversed all the serum, hepatic parameters,
Tectoridin (Figure 4) is an isoflavone glycoside
and fatty liver changes by inhibiting maturation of
isolated from the flower of P. lobata and considered
activating sterol regulatory element-binding protein 1c
as an active component in liver protection. The
(SREBP-1c) (Yin et al., 2009b).
hepatoprotective activity of tectoridin has been
Honokiol and magnolol (Figure 5) are isomers
experimentally shown on tert-butyl hyperoxide-
of biphenolic compounds isolated from MOC. In
induced hepatotoxicity in mice (Lee et al., 2005).
Lieber-DeCarli alcohol diet-fed Wistar rats, daily
Recently, it was demonstrated that tectoridin prevented
administration of honokiol (10 mg/kg bw ) exerted
acute alcohol-induced liver steatosis in C57BL/6
efficacious abrogation of fat accumulation in the liver
mice (Xiong et al., 2010). Treatment of 50 mg/kg
and completely reversed the effects on hepatotoxicity
bwtectoridin significantly alleviated the over-production
markers, including decreased hepatic glutathione and
of thiobarbituric acid-reactive substance. Furthermore,
increased hepatic triglyceride and serum TNF-α. In
tectoridin inhibited the reduction of peroxisome
addition, honokiol (10 μg/ml) reversed the production
proliferator-activated receptor-α (PPARα) expression
of lipid droplets in alcohol-treated H4IIEC3 cells.
and its target genes, including medium-chain acyl-CoA
The investigation of mechanisms demonstrated that
dehydrogenase (MCAD), acyl-CoA oxidase (ACO) and
honokiol inhibited the maturation of SREBP-1c and its
cytochrome P450 4A (CYP 4A) at mRNA and enzyme
translocation to the nucleus, the binding of nSREBP-
1c to SRE or SRE-related sequences of its lipogenic
target genes, and the expression of genes for fatty
acid synthesis. In contrast, magnolol had no effect on
nSREBP-1c levels (Yin et al., 2009c).

Figure 4. Structure of tectoridin from Puerariae lobata Figure 5. Structures of honokiol and magnolol from Magnolia
officinalis


 Lu et al . / Journal of Traditional and Complementary Medicine 2 (2012) 115-122

Platycodonis Radix (桔梗 jié gěng; the root of triglyceride level (Khanal et al., 2009a). In Lieber-
Platycodon grandiflorum A. DC, Campanulaceae) DeCarli alcohol diet-fed Sprague–Dawley rats, the
Platycodonis Radix (PR) is used as a food additive possible hepatoprotective mechanisms of CKS treatment
and has been employed for treatment of inflammatory (1 mg/kg bw/day for 2 weeks) in alcohol-induced
diseases and geriatric diseases such as bronchitis, liver damage were done through reduction of CYP2E1
asthma and pulmonary tuberculosis in TCM (Guo et expression, recovery of AMP-activated protein kinase-
al., 2007). The protective effects of PR on the liver alpha (AMPKα) phosphorylation, and an increase in
have been demonstrated in rats with alcohol-induced acetyl-CoA carboxylase phosphorylation (Khanal et al.,
hepatotoxicity. Administration of PR significantly 2009b).
prevented alcohol-induced elevation of serum and liver
Trigonellae Semen (胡蘆巴 hú lú bā; the seed of
lipids by normalizing hepatic liver fatty acid binding
Trigonella foenum-graecum , Leguminosea)
protein (L-FABP) expression and cytochrome P450 2E1
Tr i g o n e l l a f o e n u m - g r a e c u m , a l s o k n o w n a s
(CYP2E1) activity in alcohol-treated Sprague-Dawley
Fenugreek, is an annual herb and has a long history
rats (Kim et al., 2007). A recent study also reported
as both a culinary and medicinal herb. In Asia, seeds
that PR (both the total extract and saponin fraction) had
of this herb are commonly used as a spice in food
protective effects against alcohol-induced damage in
preparations due to the strong aroma and flavor.
vitro and in vivo (Noh et al., 2011). The heptoprotective
Trigonellae Semen possesses restorative and nutritive
mechanism of PR is by inhibition of lipid accumulation
properties and has been used in remedies for diabetes
and peroxidation through the enhancement of the
and hypercholesterolemia in Indian, Arabic and
antioxidant defense system such as significant decrease
Chinese medicine. (Khosla et al., 1995; Sharma et al.,
of glutamic oxalacetic transaminase, glutamic pyruvic
1990; Sharma et al., 1996). Aqueous extract (1%) of
transaminase, hepatic triglyceride and thiobarbituric
Trigonellae Semen (2 ml, twice daily) was reported to
acid reactive substance levels.
offer a significant protection against ethanol toxicity in
Saponins (Figure 6) isolated from the PR (Changkil
Wistar rats by enhancement of the antioxidant potential
saponins, CKS) were reported to be the active
and prevention of the enzymatic leakage and the rise in
components in hepatoprotective effects. To obtain
lipid peroxidation (Thirunavukkarasu et al., 2003).
saponin fraction, aqueous extract of Platycodonis
Further studies indicated that the polyphenolic extract
Radix was subjected to column chromatography to
of Trigonellae Semen was considered cytoprotective
remove saccharides and amino acids (Tada et al.,
during alcohol-induced liver damage in vitro and in
1975). In vivo studies showed that pretreatment with
vivo . Treatment of 20 to 60 μg/ml Trigonellae Semen
CKS (1 mg/kg bw/day for 7 days) prior to ethanol
polyphenol extract (FPEt) prevented alcohol-induced
administration significantly prevented alcoholic liver
toxicity and apoptosis in human Chang liver cells
injury in C57BL/6 mice by inhibiting the increases in
by reducing thiobarbituric acid reactive substance
serum alanine aminotransferase activity (ALT), hepatic
formation and decreasing the accumulation of sub-G1
TNF-α level, hepatic lipid peroxidation, and hepatic
phase cells (Kaviarasan et al., 2006). Moreover, FPEt
ameliorated the pathological liver changes induced by
chronic alcohol feeding in Wistar rats. Administration
of FPEt a dose of 200 mg/kg bw/day significantly
improved lipid profile and reduced collagen content,
aldehyde content and peroxidation (Kaviarasan et al.,
2007). Furthermore, the protective effects of FPEt in
alcoholic fatty liver diseases may involve in reducing
the levels of lipid peroxidation products and protein
carbonyl content, increasing the activities of antioxidant
enzymes, and restoring the levels of thiol groups such as
protein and non-protein thiols (Kaviarasan et al., 2008).

Figure 6. Structure of saponin from Platycodon grandiflorum


 Lu et al . / Journal of Traditional and Complementary Medicine 2 (2012) 115-122

Conclusion stress and lipogenesis, and enhancement of intestinal

permeability. Hence, the evidenced therapeutic potential
Herbal medicines have been used in China for more
of these herbs suggests that Chinese herbal medicines
than 2,000 years. However, Chinese herbal medicines
may be good resources for prevention and development
did not receive extensive analytical attention through
of new drugs for ALD in the future.
western scientific methods until recent decades. In
this review, ten herbal medicines traditionally used in
Chinese Materia Medica have been experimentally Acknowledgements
demonstrated by modern in vitro and in vivo studies The authors gratefully acknowledge Prof. Yuan-Shiun
on alcohol-induced liver injury. As shown in Table 1, Chang for providing the elegant photos of Chinese
the potentially protective mechanisms of these herbs in Materia Medica, and Mr. Eric Te-Yu Chen for his very
alcoholic liver disease are involved in amelioration of kind editorial assistance.
enhanced inflammation, reduction of hepatic oxidative

Table 1. Hepatoprotective effect of Chinese herbal medicine against alcoholic liver disease

Chinese Materia Medica Experimental model Treatment Proposed mechanism (reference)

Salviae Miltiorrhizae Radix Hepatic cells in SMR extract Decreased TLR-4 & HO-1 levels; decreased TLR-4
丹參 (dān shēn) Kunming mice (5 ml/kg bw, i.p.) positive cell number
(Xiong et al., 2005)
Primary rat hepatocytes Cryptotanshinone Inhibited activation and nuclear translocation of
(10 μM) SREBP-1
(Yin et al., 2009a)
RAW 264.7 cells Tanshinone IIA Reversed of CD14, iNOS, & SCD1
(10 μM) (Yin et al., 2008)
Rat hepatoma cells Tanshinone IIA Reduced alcohol-induced Kupffer cell sensitization;
(H4IIEC3) (10 μM) decreased synthesis of reactive oxygen/nitrogen
species & fatty acid synthesis; stimulated fatty acid
oxidation
(Yin et al., 2008)

Notoginseng Radix ICR Mice PNG Increased sGOT, AST, sGPT, ALT; inhibited hepatic
三七 (sān qī) (10 mg/kg bw, p.o.) lipid peroxidation
(Lin et al., 2003)

Lycii Fructus Rats LBP Decreased AST, ALT; increased antioxidant activity
枸杞子 (gǒu qǐ zǐ) (300 mg/kg bw) (Cheng and Kong, 2011)

Cnidii Fructus Kunming Mice Osthole Reduced hepatic oxidative stress; enhanced
蛇床子 (shé chuáng zǐ) (40 mg/kg bw, p.o.) antioxidative enzyme activity; reduced lipid
accumulation & peroxidation, down-regulation of
gene expressions of DGAT, HMG-CoA reductase
and CYP7A mediated by increasing the PPARα
mRNA expression
(Sun et al., 2009)

Gentianae Radix C57BL/6 mice GM Suppressed elevated MDA; restored GSH level;
龍膽 (lóng dǎn) (200 mg/kg bw) enhanced SOD, CAT and GPx activities; blocked
CYP2E1-mediated free radical scavenging and
SREBP-1-regulated fatty acid synthesis
(Lian et al., 2010)

Puerariae Radix Sprague-Dawley rats Water extracts of PR and PF Normalized antioxidant enzymes, including
葛根 (gé gēn) / (1.2 g of raw PR or PF/kg increased Cu/Zn SOD and/or CAT, decreased GPx
bw/day) activity
(Lee et al., 2001)
Sprague-Dawley rats Water extracts of PR Enhanced lipid metabolism and hepatic antioxidant
(1.5 g of raw PR/kg bw/day) defense system
(Lee, 2004)
Puerariae Flos Wistar rats 3 g of raw PR/kg bw/day, Enhanced intestinal permeability to improve
葛花 (gé huā) p.o. intestinal barrier dysfunction
(Zhang et al., 2009)
C57BL/6 mice Tectoridin Modulated the disturbance of PPARα pathway and
(50 mg/kg bw) ameliorated mitochondrial function
(Xiong et al., 2010)


 Lu et al . / Journal of Traditional and Complementary Medicine 2 (2012) 115-122

Chinese Materia Medica Experimental model Treatment Proposed mechanism (reference)

Magnoliae Officinalis Cortex Wistar rats Ethanolic extract of MOC Inhibited maturation of SREBP-1c
厚朴 (hòu pò) (45 mg/kg bw/day) (Yin et al., 2009b)
RAW264.7 cells Ethanolic extract of MOC Decreased production of TNF-α, ROS and SOD
(50 μg/ml) anion radicals; inhibits NADPH oxidase activation
(Yin et al., 2009b)
Wistar rats Honokiol Inhibition of SREBP-1c protein maturation and of
(10 mg/kg bw) the expression of Srebf1c and its target genes for
hepatic lipogenesis
(Yin et al., 2009c)
H4IIEC3 cells Honokiol Inhibited maturation of SREBP-1c and its
(10 μg/ml) translocation to the nucleus; the binding of nSREBP-
1c to SRE or SRE-related sequences of its lipogenic
target genes, and the expression of genes for fatty
acid synthesis
(Yin et al., 2009c)

Platycodonis Radix Sprague-Dawley rats Metholic extract of PR Normalized L-FABP expression and CYP2E1
桔梗 (jié gěng) (diet with 0.15% PR) (Kim et al., 2007)
C57BL/6 mice Total extract and saponin Enhanced antioxidant defense system such as
fraction of PR significant decrease of ALT, AST, hepatic TG,
TBARS levels
(Noh et al., 2011)
C57BL/6 mice CKS Inhibited increases in serum ALT, hepatic TNF-α,
(1 mg/kg bw/day) hepatic lipid peroxidation and hepatic triglyceride
level
(Khanal et al., 2009a)
Sprague-Dawley rats CKS Reduced CYP2E1 expression; recovered AMPKα
(1 mg/kg bw/day for 2 phosphorylation; increased ACC phosphorylation
weeks) (Khanal et al., 2009b)

Trigonellae Semen Wistar rats 1% aqueous extract of TS Enhanced antioxidant potential; prevented enzymatic
胡蘆巴 (hú lú bā) (2 ml, twice daily) leakage; increased lipid peroxidation
(Thirunavukkarasu et al., 2003)
Chang liver cells Polyphenolic extract of TS Reduced TBARS formation and decreased
(20 to 60 μg/ml) accumulation of sub-G1 phase cells
(Kaviarasan et al., 2006)
Wistar rats Polyphenolic extract of TS Reduced collagen content; aldehyde content and
(200 mg/kg bw/day) peroxidation
(Kaviarasan et al., 2007)

Chang liver cells. Alcohol & Alcoholism 41, 267-273.

References
Kaviarasan, S., Sundarapandiyan, R., Anuradha, C.V., 2008. Protective
An, L., Wang, X., Cederbaum, A.I., 2012. Cytokines in alcoholic liver action of fenugreek (Trigonella foenum-graecum ) seed polyphenols
disease. Archives of Toxicology. DOI: 10.1007/s00204-012-0814-6 against alcohol-induced protein and lipid damage in rat liver. Cell
Bondy, S.C., 1992. Ethanol toxicity and oxidative stress. Toxicology Biology and Toxicology 24, 391-400.
Letters 63, 231-241. Kaviarasan, S., Viswanathan, P., Anuradha, C.V., 2007. Fenugreek
Cheng, D., Kong, H., 2011. The effect of Lycium barbarum seed (Trigonella foenum-graecum ) polyphenols inhibit ethanol-
polysaccharide on alcohol-induced oxidative stress in rats. induced collagen and lipid accumulation in rat liver. Cell Biology
Molecules 16, 2542-2550. and Toxicology 23, 373-383.
Chien, C.F., Wu, Y.T., Tsai, T.H., 2011. Biological analysis of herbal Keung, W.M., Vallee, B.L., 1998. Kudzu root: an ancient Chinese
medicines used for the treatment of liver diseases. Biomedical source of modern antidipsotropic agents. Phytochemistry 47,
Chromatography 25, 21-38. 499-506.
Feng, Y., Cheung, K.F., Wang, N., Liu, P., Nagamatsu, T., Tong, Y., Khanal, T., Choi, J.H., Hwang, Y.P., Chung, Y.C., Jeong, H.G., 2009a.
2009. Chinese medicines as a resource for liver fibrosis treatment. Saponins isolated from the root of Platycodon grandiflorum protect
Chinese Medicine 4, 16. against acute ethanol-induced hepatotoxicity in mice. Food and
Fogden, E., Neuberger, J., 2003. Alternative medicines and the liver. Chemical Toxicology 47, 530-535.
Liver International 23, 213-220. Khanal, T., Choi, J.H., Hwang, Y.P., Chung, Y.C., Jeong, H.G.,
Guo, L., Zhang, C., Li, L., Xiao, Y.Q., 2007. Advances in studies on 2009b. Protective effects of saponins from the root of Platycodon
Platycodon grandiflorum (Chinese). China Journal of Chinese grandiflorum against fatty liver in chronic ethanol feeding via the
Materia Medica 32, 181-186. activation of AMP-dependent protein kinase. Food and Chemical
Haber, P.S., Warner, R., Seth, D., Gorrell, M.D., McCaughan, G.W., Toxicology 47, 2749-2754.
2003. Pathogenesis and management of alcoholic hepatitis. Journal Khosla, P., Gupta, D.D., Nagpal, R.K., 1995. Effect of Trigonella
of Gastroenterology and Hepatology 18, 1332-1344. foenum-graecum (Fenugreek) on blood glucose in normal and
Kaviarasan, S., Ramamurty, N., Gunasekaran, P., Varalakshmi, E., diabetic rats. Indian Journal of Physiology and Pharmacology 39,
Anuradha, C.V., 2006. Fenugreek (Trigonella foenum-graecum ) 173-174.
seed extract prevents ethanol-induced toxicity and apoptosis in Kim, H.K., Kim, D.S., Cho, H.Y., 2007. Protective effects of Platycodi


 Lu et al . / Journal of Traditional and Complementary Medicine 2 (2012) 115-122

radix on alcohol-induced fatty liver. Bioscience, Biotechnology, PPAR alpha-mediated lipogenic gene expression in alcoholic fatty
and Biochemistry 71, 1550-1552. liver murine. Phytomedicine 17, 669-673.
Lee, H.U., Bae, E.A., Kim, D.H., 2005. Hepatoprotective effect of Sun, F., Xie, M.L., Zhu, L.J., Xue, J., Gu, Z.L., 2009. Inhibitory effect
tectoridin and tectorigenin on tert-butyl hyperoxide-induced liver of osthole on alcohol-induced fatty liver in mice. Digestive and
injury. Journal of Pharmacological Sciences 97, 541-544. Liver Disease 41, 127-133.
Lee, J.S., 2004. Supplementation of Pueraria radix water extract on Sun, J., Huang, S.H., Tan, B.K., Whiteman, M., Zhu, Y.C., Wu, Y.J.,
changes of antioxidant enzymes and lipid profile in ethanol-treated Ng, Y., Duan, W., Zhu, Y.Z., 2005. Effects of purified herbal extract
rats. Clinica Chimica Acta 347, 121-128. of Salvia miltiorrhiza on ischemic rat myocardium after acute
Lee, K.H., Morris-Natschke, S., Qian, K., Dong, Y., Yang, X., Zhou, myocardial infarction. Life Sciences 76, 2849-2860.
T., Belding, E., Wu, S.F., Wada, K., Akiyama, T., 2012. Recent Tada, A., Kaneiwa, Y., Shoji, J., Shibata, S., 1975. Studies on the
progress of research on herbal products used in traditional Chinese saponins of the root of Platycodon grandiflorum A. De Candolle.
medicine: the herbs belonging to the Divine Husbandman’s Herbal I. Isolation and the structure of platycodin-D. Chemical &
Foundation Canon (神農本草經 Shén Nóng Běn Cǎo Jīng). Journal Pharmaceutical Bulletin 23, 2965-2972.
of Traditional and Complementary Medicine 2, 6-26. Thirunavukkarasu, V., Anuradha, C.V., Viswanathan, P., 2003.
Lee, M.K., Cho, S.Y., Jang, J.Y., Cho, M.S., Jeon, S.M., Jang, Protective effect of fenugreek (Trigonella foenum-graecum )
M.K., Kim, M.J., Park, Y.B., 2001. Effects of Puerariae Flos and seeds in experimental ethanol toxicity. Phytotherapy Research 17,
Puerariae Radix extracts on antioxidant enzymes in ethanol-treated 737-743.
rats. The American Journal of Chinese Medicine 29, 343-354. Wang, A.Y., Lian, L.H., Jiang, Y.Z., Wu, Y.L., Nan, J.X., 2010.
Lee, Y.J., Lee, Y.M., Lee, C.K., Jung, J.K., Han, S.B., Hong, J.T., Gentiana manshurica Kitagawa prevents acetaminophen-induced
2011. Therapeutic applications of compounds in the Magnolia acute hepatic injury in mice via inhibiting JNK/ERK MAPK
family. Pharmacology & Therapeutics 130, 157-176. pathway. World Journal of Gastroenterology 16, 384-391.
Lei, X.L., Chiou, G.C., 1986. Studies on cardiovascular actions of Wang, N., Luo, H.W., Niwa, M., Ji, J., 1989. A new platelet
Salvia miltiorrhiza. The American Journal of Chinese Medicine 14, aggregation inhibitor from Salvia miltiorrhiza. Planta Medica 55,
26-32. 390-391.
Lian, L.H., Wu, Y.L., Song, S.Z., Wan, Y., Xie, W.X., Li, X., Bai, T., World Health Organization, 2011. Global Status Report on Alcohol
Ouyang, B.Q., Nan, J.X., 2010. Gentiana manshurica Kitagawa and Health. WHO Press, Switzerland.
reverses acute alcohol-induced liver steatosis through blocking Wu, D., Cederbaum, A.I., 2005. Oxidative stress mediated toxicity
sterol regulatory element-binding protein-1 maturation. Journal of exerted by ethanol-inducible CYP2E1. Toxicology and Applied
Agricultural and Food Chemistry 58, 13013-13019. Pharmacology 207, 70-76.
Lian, Q., 2003. Advances in the study of chemical constituents Xiong, Y., Yang, Y., Yang, J., Chai, H., Li, Y., Jia, Z., Wang, Z., 2010.
and pharmacological actions of Cnidium monnieri (L.) Cusson Tectoridin, an isoflavone glycoside from the flower of Pueraria
(Chinese). Journal of Chinese Medicinal Materials 26, 141-144. lobata, prevents acute ethanol-induced liver steatosis in mice.
Lin, C.F., Wong, K.L., Wu, R.S., Huang, T.C., Liu, C.F., 2003. Toxicology 276, 64-72.
Protection by hot water extract of Panax notoginseng on chronic Xiong, Z.B., Wu, P., Huang, Y.F., 2005. Protective mechanisms of
ethanol-induced hepatotoxicity. Phytotherapy Research 17, radix Salviae miltiorrhizae against chronic alcoholic liver injury
1119-1122. in mice (Chinese). Chinese Journal of Integrated Traditional and
Ng, T.B., 2006. Pharmacological activity of sanchi ginseng (Panax Western Medicine 25, 425-428.
notoginseng ). The Journal of Pharmacy and Pharmacology 58, Yin, H.Q., Choi, Y.J., Kim, Y.C., Sohn, D.H., Ryu, S.Y., Lee, B.H.,
1007-1019. 2009a. Salvia miltiorrhiza Bunge and its active component
Noh, J.R., Kim, Y.H., Gang, G.T., Hwang, J.H., Kim, S.K., Ryu, S.Y., cryptotanshinone protects primary cultured rat hepatocytes from
Kim, Y.S., Lee, H.S., Lee, C.H., 2011. Hepatoprotective effect of acute ethanol-induced cytotoxicity and fatty infiltration. Food and
Platycodon grandiflorum against chronic ethanol-induced oxidative Chemical Toxicology 47, 98-103.
stress in C57BL/6 mice. Annals of Nutrition & Metabolism 58, Yin, H.Q., Je, Y.T., Kim, Y.C., Shin, Y.K., Sung, S., Lee, K., Jeong,
224-231. G.S., Lee, B.H., 2009b. Magnolia officinalis reverses alcoholic
Okamoto, T., Kawasaki, T., Hino, O., 2003. Osthole prevents anti- fatty liver by inhibiting the maturation of sterol regulatory element-
Fas antibody-induced hepatitis in mice by affecting the caspase- binding protein-1c. Journal of Pharmacological Sciences 109,
3-mediated apoptotic pathway. Biochemical Pharmacology 65, 486-495.
677-681. Yin, H.Q., Kim, Y.S., Choi, Y.J., Kim, Y.C., Sohn, D.H., Ryu, S.Y.,
Okamoto, T., Kobayashi, T., Yoshida, S., 2005. Chemical aspects Lee, B.H., 2008. Effects of tanshinone IIA on the hepatotoxicity
of coumarin compounds for the prevention of hepatocellular and gene expression involved in alcoholic liver disease. Archives
carcinomas. Current medicinal chemistry. Anti-cancer Agents 5, of Pharmacal Research 31, 659-665.
47-51. Yin, H.Q., Kim, Y.C., Chung, Y.S., Shin, Y.K., Lee, B.H., 2009c.
Pan, M.H., Chiou, Y.S., Tsai, M.L., Ho, C.T., 2011. Anti-inflammatory Honokiol reverses alcoholic fatty liver by inhibiting the maturation
activity of traditional Chinese medicinal herbs. Journal of of sterol regulatory element binding protein-1c and the expression
Traditional and Complementary Medicine 1, 8-24. of its downstream lipogenesis genes. Toxicology and Applied
Seth, D., Hogg, P.J., Gorrell, M.D., McCaughan, G.W., Haber, P.S., Pharmacology 236, 124-130.
2008. Direct effects of alcohol on hepatic fibrinolytic balance: You, M., Crabb, D.W., 2004. Recent advances in alcoholic liver
implications for alcoholic liver disease. Journal of Hepatology 48, disease II. Minireview: molecular mechanisms of alcoholic fatty
614-627. liver. American Journal of Physiology. Gastrointestinal and Liver
Sharma, R.D., Raghuram, T.C., Rao, N.S., 1990. Effect of fenugreek Physiology 287, G1-6.
seeds on blood glucose and serum lipids in type I diabetes. You, M., Fischer, M., Deeg, M.A., Crabb, D.W., 2002. Ethanol
European Journal of Clinical Nutrition 44, 301-306. induces fatty acid synthesis pathways by activation of sterol
Sharma, R.D., Sarkar, A., Hazra, D. K., Misra, B., Singh, J. B., regulatory element-binding protein (SREBP). The Journal of
Maheshwari, B. B., Sharma, S. K., 1996. Hypolipidaemic effect of Biological Chemistry 277, 29342-29347.
fenugreek seeds: a chronic study in non-insulin dependent diabetic Zhang, J., Xue, J., Wang, H., Zhang, Y., Xie, M., 2011. Osthole
patients. Phytotherapy Research 10, 332-334. improves alcohol-induced fatty liver in mice by reduction of
Stewart, S., Jones, D., Day, C.P., 2001. Alcoholic liver disease: new hepatic oxidative stress. Phytotherapy Research 25, 638-643.
insights into mechanisms and preventative strategies. Trends in Zhang, R., Hu, Y., Yuan, J., Wu, D., 2009. Effects of Puerariae Radix
Molecular Medicine 7, 408-413. extract on the increasing intestinal permeability in rat with alcohol-
Sun, F., Xie, M.L., Xue, J., Wang, H.B., 2010. Osthol regulates hepatic induced liver injury. Journal of Ethnopharmacology 126, 207-214.