Wound Healing In Diabetic Patients

Delayed wound healing is one of the complications of diabetes mellitus. The present study was performed to investigate the effect of Aloe vera oral administration on open wounds in type 2 diabetic rats. Full thickness open wounds (1.5  1.5 cm) were created under general anesthesia on the backs of the rats. These rats were divided into two group, a control group (Group C) and an Aloe vera oral administration group (Group A). Each wound area was measured on days 1, 2, 4 and 8 postwounding. The stages of wound granulation tissues were evaluated histopathologically. The expression of transforming growth factor (TGF)-1 and vascular endothelial growth factor (VEGF) were determined by immunohistochemically. The wounds were significantly contracted in Group A on days 2, 4 and 8 postwounding. Histological results revealed that the inflammatory cell infiltration, angiogenesis, extracellular matrix deposition and epithelialization were promoted in Group A, respectively. The immunohistochemical results revealed that both TGF-1 and VEGF protein-positive cells increased in Group A on day 4 postwounding. We concluded that Aloe vera oral administration accelerated wound healing in type 2 diabetic rats.

Chronic ulcers represent a major health problem in diabetic patients resulting in pain and discomfort. Conventional therapy does not guarantee adequate wound repair. In diabetes, impaired healing is partly due to poor endothelial progenitor cells mobilisation and homing, with altered levels of the chemokine stromal-derived factor-1 (SDF-1) at the wound site. Adipose tissue-associated stromal cells (AT-SCs) can provide an accessible source of progenitor cells secreting proangiogenic factors and differentiating into endothelial-like cells. We demonstrated that topical administration of AT-SCs genetically modified ex vivo to overexpress SDF-1, promotes wound healing into diabetic mice. In particular, by in vivo bioluminescent imaging analysis, we monitored biodistribution and survival after transplantation of luciferase-expressing cells. In conclusion, this study indicates the therapeutic potential of AT-SCs administration in wound healing, through cell differentiation, enhanced cellular recruitment at the wound site, and paracrine effects associated with local growth-factors production.

Manuka honey has attracted the attention of the scientific community
for its antimicrobial and antioxidant properties. The active compounds of manuka honey to which its myeloperoxidase activity inhibition is owed are methyl syringate (MSYR) and leptosin (a novel glycoside of MSYR). The non-peroxide antibacterial activity is attributed to glyoxal, 3 deoxyglucosulose, and methylglyoxal. These properties make it an inexpensive and effective topical treatment in wound management. This study has focused on the evaluation of the effect of manuka honey and acacia honey on wound healing in nondiabetic and streptozotocin-induced diabetic rats. Materials and Methods: This study was conducted on a total of 42 rats (six rats in each group) and respective drug/substance was topically applied once daily on the excision wound for 21 days. Induction of diabetes was carried out in rats in groups IV, V, VI, and VII only. Measurement of wound contraction was carried out on days 3, 6, 9, 12, 15, 18, and 21 after operation. Time taken for the complete epithelization was recorded along with a histopathological examination of the healed wound bed. Results: Topical application of manuka honey achieved ≥80% wound contraction on day 9 after operation in both the nondiabetic and diabetic group. Complete epithelization was achieved 2 days earlier than the normal epithelization time in the manuka group. Histopathological examination showed well-formed keratinized squamous epithelium with normal collagen tissue surrounding hair follicles. Conclusion: This study provides good outcome with respect to wound healing (especially in diabetic condition) when manuka honey was compared to acacia honey and standard treatment.

Metadichol ® is a nano formulation of long-chain lipid alcohols derived from food It is a inverse agonist of Vitamin
D receptor (VDR), Aryl hydrocarbon receptor (AHR), and ROR gamma (RORC) that could have beneficial effects on
skin diseases. We now present case studies of patients with various skin diseases who has symptoms mitigated on
treatment with Metadichol. The proposed mechanism is that Metadichol by its actions on the above mentioned
nuclear receptors affects Th1, TH2,Th 17, IL 17 and IL22 and IL 23 pathways that exacerbate many Skin diseases.
Metadichol is the first molecule to successfully navigate around the problems involved with promiscuous ligands
and targets. It fulfills the goals of the emerging field of Polypharmacology i.e a single drug is able to bind to multiple
targets beyond the "one drug, one target" concept. We show how Metadichol is an innovative treatment for treating
multiple skin diseases like eczema, acne, diabetic wounds viral and bacterial infection and also improving skin
texture. Metadichol ® is a safe non toxic low cost solution and is an alternative to numerous clinical candidates in
combating over 3000 skin diseases.