三羟基异黄酮诱导增生性瘢痕成纤维细胞凋亡及其机制研究  

The study of the apoptosis induction and mechanism of Genistein on the human hyperplastic scar fibroblasts

作　　者：曹川[1] 李世荣[1] 冯智[1] 陈艳清[1] 夏珊[1] 姚恒[1] 陶灵[1] 覃霞[1] 

机构地区：[1]第三军医大学西南整形美容外科医院,重庆400038

出　　处：《中国美容医学》2007年第5期600-603,共4页Chinese Journal of Aesthetic Medicine

摘　　要：目的:探讨三羟基异黄酮(Genistein)诱导体外培养的人增生性瘢痕成纤维细胞凋亡的作用及相关机制。方法:体外分离培养人增生性瘢痕成纤维细胞,不同浓度Genistein作用后,MTT比色法检测细胞增殖情况,流式细胞术检测细胞凋亡情况,Western Blot法检测细胞Bcl-2、Bax、Caspase-3蛋白表达。结果:在Genistein作用下,增生性瘢痕成纤维细胞的生长受到抑制;细胞凋亡率增加,与对照组相比具有显著性差异(P<0.05);Bcl-2的表达下调、Bax、Caspase-3表达增加。结论:Genistein可通过诱导凋亡抑制增生性瘢痕成纤维细胞增殖,其作用机制可能与影响Bcl-2、Bax、Caspase-3等凋亡调控基因的表达有关。Objective To explore the apoptosis induction and mechanism of Genistein on the human hyperplastic scar fibroblasts in vitro. Methods The human hyperplastic scar fibroblasts were cultured in vitro and disposed with Genistein. The cells＂ proliferation was measured with MTT colorimetric method. The cells＂ apoptosis was assessed by flowing cytometry. The expression of Bcl-2,Bax,Caspase-3 protein were detected by Western Blot. Results Under the Genistein con-culture, the cells＂ proliferation was markedly inhibited with a higher cell apoptosis rate compared with control group （P〈0.05）. The expression of Bcl-2 protein was reduced but Bax, Caspase-3＇s expression were up-regulated. Conclusion Genistein can inhibit the proliferation of hyperplastic scar fibroblasts by inducing cell apoptosis, the mechanism of which may be Genistein＇s effect on the expression of Bcl-2, Bax,Caspase-3.

关 键 词：三羟基异黄酮 增生性瘢痕 凋亡 BCL-2 BAX CASPASE-3 

分 类 号：Q813.1[生物学—生物工程]