Topical buspirone accelerates wound healing in rats through modulation of inflammation, angiogenesis, and collagen formation

Abstract

Objective(s): Cutaneous wound healing is a complex, multistep process that requires coordinated regulation of inflammation, cell proliferation, extracellular matrix deposition, and angiogenesis. This study evaluated the effects of topical buspirone, a partial 5-HT1A receptor agonist, on wound healing in a rat excisional wound model. Materials and Methods: Full-thickness dorsal wounds were created in Wistar rats and treated with topical 0.5% buspirone, 1% phenytoin, vehicle, or left untreated. Wound contraction was assessed macroscopically, and hydroxyproline content, TNF-α, and TGF-β levels were measured to evaluate collagen deposition and inflammatory and fibrotic responses. Histopathological analysis and a chick chorioallantoic membrane (CAM) assay were also performed. Results: Buspirone treatment significantly accelerated wound contraction at all time points compared with the control, vehicle, and phenytoin groups (P<0.001). Hydroxyproline levels were significantly increased, indicating enhanced collagen deposition. In addition, TNF-α levels were reduced, whereas TGF-β levels showed a moderate increase, suggesting balanced modulation of inflammation and fibrosis. Histological findings demonstrated improved re-epithelialization and dermal organization in the buspirone-treated group. Enhanced angiogenesis was also observed in the CAM assay. Conclusion: Overall, topical buspirone may promote wound healing through coordinated effects on inflammation, collagen synthesis, tissue organization, and angiogenesis. This suggests that buspirone is a potential therapeutic agent for wound healing.