没食子酸体外诱导人肝癌SMMC-7721细胞凋亡的作用机制

Effect of gallic acid on apoptosis of human hepatocellular carcinoma SMMC-7721cells and its possible mechanism

目的探讨没食子酸（gallicacid，GA）对人肝癌SMMC-7721细胞凋亡的影响及其可能的作用机制。方法没食子酸干预SMMC-7721细胞后，MTT法检测其对细胞生长抑制的影响，计算IC50值；DNA琼脂糖凝胶电泳观察SMMC-7721细胞DNA降解情况；流式细胞仪检测细胞凋亡；Westernblot检测相关蛋白表达。结果GA作用SMMC-7721细胞48h的IC50为（31.2±1.8）μg/mL；12.5、25、50μg/mLGA作用SMMC-7721细胞48h后，细胞DNA电泳可见典型的DNA凋亡梯状条带；GA各剂量组SMMC-7721细胞线粒体膜电位降低，峰值明显左移；GA激活了SMMC-7721细胞的caspase-3及9凋亡通路，上调促凋亡蛋白Bax的表达。结论GA可能通过线粒体凋亡途径诱导SMMC-7721细胞的凋亡，抑制肝癌SMMC-7721细胞的增殖。

Objective To investigate the effect of gallic acid on the apoptosis of human hepatocellular carcinoma SMMC-7721cells and its possible mechanism.Methods DNA activity was measured by DNA agarose gel electrophoresis.The DNA degradation of SMMC-7721cells was observed by flow cytometry.The apoptosis of SMMC-7721cells was detected by flow cytometry.The expression of IC50was detected by MTT assay.Western blot to detect the expression of related proteins.Results The IC50of SMMC-7721cells treated with GA was(31.2±1.8)μg/mL;12.5,50,50μg/mL GA for48h after SMMC-7721cells,the typical DNA apoptotic bands were observed by DNA electrophoresis.GA inhibited the mitochondrial membrane potential of SMMC-7721cells,and the peak value was significantly shifted to the left.GA activated the caspase-3and9apoptotic pathway of SMMC-7721cells to up-regulate the expression of pro-apoptotic protein Bax.Conclusion GA may induce the apoptosis of SMMC-7721cells by mitochondrial apoptosis and inhibit the proliferation of SMMC-7721cells.