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

OBJECTIVES

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.