The aim of the present work was to investigate the effect of BM-MSCs on wound closure in STZ-induced diabetic rats. Diabetic wound models were carried out by making a standard wound on dorsum of forty rats, which were divided into four groups with ten rats in each: Wound from diabetic and non-diabetic control rats were treated with PBS, while diabetic and non-diabetic treated rats were treated with BM-MSCs for 12 days. The closure rate and the ratios relative to the beta actin gene of both treated groups (diabetic and non-diabetic) were significantly increased at 7 and 12 days after wounding as compared to their corresponding controls (P < 0.05). Histologic analysis revealed complete reepithelialization in treated groups. Taken together, BM-MSCs mediated correction of the diabetic wound healing impairment is due to, partly, increased VEGF expression in the skin of STZ-induced diabetic rats.
