丝裂霉素C影响增生性瘢痕成纤维细胞的凋亡

背景：丝裂霉素C已逐渐开始应用于治疗增生性瘢痕领域中,但针对丝裂霉素C通过细胞凋亡作用于增生性瘢痕分子机制报道很少。目的：探讨丝裂霉素C对增生性瘢痕成纤维细胞凋亡的影响。方法：应用2.5,12.5,50,100和200mg/L丝裂霉素C作用于体外培养的增生性瘢痕成纤维细胞,采用流式细胞仪检测成纤维细胞的周期分布和凋亡情况;通过Westernblot法检测细胞中Bax和Bcl-2蛋白表达水平。结果与讨论：丝裂霉素C可使增生性瘢痕成纤维细胞的生长阻滞于G0/G1期,并且能够诱导增生性瘢痕成纤维细胞发生凋亡,有着明显的浓度依赖性。经2.5~200mg/L丝裂霉素C作用24h后,增生性瘢痕成纤维细胞中Bax蛋白表达增高,Bcl-2蛋白表达降低（P〈0.05）。说明丝裂霉素C可能通过增加增生性瘢痕成纤维细胞Bax表达,降低Bcl-2表达,促进成纤维细胞凋亡的增加。

Effects of mitomycin C on apoptosis of hypertrophic scar fibroblasts

BACKGROUND： Mitomycin C has been gradually used in hyperplastic scar therapy. But the molecular mechanism underlying the effects of mitomycin C on hyperplastic scar via cell apoptosis is reported few. OBJECTIVE： To explore the effects of mitomycin C on fibroblasts apoptosis in hypertrophic scar. METHODS： Hypertrophic scar fibroblasts were cultured in vitro with five different concentrations of mitomycin C （2.5, 12.5, 50, 100, 200 mg/L）. Cell cycle distribution and apoptosis of fibroblasts were detected by Annexin V-PI, and the protein expression levels of Bax and Bcl-2 in fibroblasts were detected with Western blotting. RESULTS AND CONCLUSION： Mitomycin C blocked the growth of hyperplastic scar fibroblasts in G0/G1 period, and induced apoptosis of hyperplastic scar fibroblasts in an obvious concentration-dependent manner. Bax protein expression levels increased and Bcl-2 protein expression levels decreased in hyperplastic scar fibroblasts after treated with 2.5-200 mg/L mitomycin C for 24 hours （P 0.05）. These findings indicate that mitomycin C has the possibility to promote fibroblasts apoptosis through increasing Bax expression and decreasing Bcl-2 expression in hyperplastic scar fibroblasts.