What is it about?
Abstract Background Delayed wound healing is a serious complication of diabetes mellitus, leading to chronic ulcers, infection, and prolonged recovery. Effective therapies are needed to improve both speed and quality of repair in diabetic conditions. Hypothesis/Aim This study evaluated whether botulinum toxin A (BTX-A) enhances healing of full-thickness skin wounds in diabetic rats. Methods In this randomised controlled study, 24 male Wistar rats were rendered diabetic with streptozotocin and assigned to two groups (n=12 each). A 20×20 mm dorsal full-thickness skin wound was created in each rat. The treatment group received 5 IU BTX-A injected intradermally around the wound; controls received saline. Wound closure was assessed on days 0, 7, 14, and 21. Histological evaluation of angiogenesis, fibroblast proliferation, collagen deposition and inflammatory infiltration was performed on days 7 and 14. Data were analysed using Prism software with significance set at P<0.05. Results/Findings By day 7, wound closure was greater in the BTX-A group (40%) compared with controls (25%). Histology showed enhanced angiogenesis, higher fibroblast counts, increased collagen content, and reduced inflammatory infiltration in the treated group. By day 21, wound healing reached 95% in the BTX-A group versus 81% in controls. No adverse effects or toxicity were observed. Conclusions BTX-A accelerated wound closure and improved tissue repair in diabetic rats. Implications for clinical practice BTX-A may offer a novel adjunctive therapy for chronic diabetic wounds, but further preclinical and clinical trials are required to confirm safety and efficacy.
Featured Image
Read the Original
This page is a summary of: Investigating the effect of botox on the secondary skin defect healing in diabetic rats, Journal of Wound Management Official journal of the European Wound Management Association, July 2026, European Wound Management Association,
DOI: 10.35279/jowm2026.27.02.10.
You can read the full text:
Contributors
The following have contributed to this page







