AI Article Synopsis
- The study explored the effects of an ointment made from gall extract on open wound healing in diabetic mice.
- The treatment resulted in decreased wound area and inflammatory markers (IL-6 and TNF-α), while enhancing healing indicators like angiogenesis and collagen production.
- Overall, the gall ointment was found to speed up the healing process by promoting antioxidant activity and regulating cell survival factors.
Article Abstract
Objective: galls have commonly been used for different therapeutic purposes. This study was conducted to investigate the effects of topical application of an ointment prepared from gall hydroethanolic extract on open wound healing in a streptozocin-induced diabetic BALB/c mouse model.
Method: After induction of diabetes, two circular wounds (5mm) were created on the dorsum of the mice which were then divided into three groups. The mice were treated with soft yellow paraffin (control-sham group) and therapeutic doses of 5% and 10% of an ointment prepared from , respectively. To evaluate the effects of the therapeutic ointment on the wound healing process, wound area, histological parameters, mRNA levels of vascular endothelial growth factor (VEGF), Bcl-2 and p53, plasma levels of interleukin-6 (IL-6) and tumour necrosis factor (TNF)-α, and tissue antioxidant capacity were investigated.
Results: The mice (n=54) were divided into three equal groups. Wound area and concentrations of IL-6 and TNF-α were significantly decreased in both ointment-treated groups compared to the control group (p<0.05). Moreover, angiogenesis, fibroblast distribution per mm of wound tissue, collagen deposition, rapid re-epithelialisation, and the expression of VEGF, Bcl-2 and p53 mRNA, were significantly increased (p<0.05). The administration of the ointment reduced malondialdehyde concentration and increased total antioxidant capacity compared with the control group (p<0.05).
Conclusion: Our study suggests that an ointment prepared from gall hydroethanolic extract accelerated open wound healing in a diabetic animal model by shortening the inflammatory phase, inducing apoptosis, up-regulating the expression of Bcl-2 and p53 mRNA, antioxidant properties and cellular proliferation.
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| http://dx.doi.org/10.12968/jowc.2021.30.8.618 | DOI Listing |
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