RESUMO
BACKGROUND: Clinical observations indicate that Botulinum toxin type A (BTXA) can inhibit the growth and improve the eventual appearance of hypertrophic scarring. However, the molecular mechanism remains unclear. OBJECTIVE: We used human keloid fibroblasts to investigate the molecular mechanism of BTXA on hypertrophic scarring. METHODS: Different concentrations of BTXA (0.01, 0.1, 1, and 10 U/L) were used to treat keloid fibroblasts. Changes in cellular morphology, viability, proliferation, cell cycle, and apoptosis were observed by immunofluorescence, MTT assay, and flow cytometry. In addition, real-time qPCR and Western blotting were used to explore the potential molecular mechanisms. RESULTS: Keloid fibroblast viability decreased with increasing BTXA dose. After BTXA treatment, the volume of keloid fibroblasts cells increased, but the nucleus of cells shrunk. Long thin dendrites were formed as the concentration of BTXA increased. Furthermore, the proliferation and S phase of keloid fibroblasts were inhibited by BTXA. Matrix metalloproteinase (, MMP)-1 and -2 RNA and protein showed high expression, but TGF-ß1 and MMP-9 showed low expression than the control. CONCLUSION: Botulinum toxin type A may promote the healing of scars by inhibiting the proliferation of keloid fibroblasts and regulating the expression of TGF-ß1, which could affect the expression of MMP-1 and MMP-2. This study provides theoretical support for the clinical application of BTXA to control hypertrophic scarring.
