没食子酸体外诱导人肝癌SMMC-7721细胞凋亡的作用机制

摘要

Objective To investigate the effect of gallic acid on the apoptosis of human hepatocellular carcinoma SMMC-7721 cells and its possible mechanism. Methods DNA activity was measured by DNA agarose gel electrophoresis. The DNA degradation of SMMC-7721 cells was observed by flow cytometry. The apoptosis of SMMC-7721 cells was detected by flow cytometry. The expression of IC50 was detected by MTT assay. Western blot to detect the expression of related proteins. Results The IC50 of SMMC-7721 cells treated with GA was (31.2 ± 1.8) μg/mL;12.5, 50, 50 μg/mL GA for 48 h after SMMC-7721 cells, the typical DNA apoptotic bands were observed by DNA electrophoresis. GA inhibited the mitochondrial membrane potential of SMMC-7721 cells, and the peak value was significantly shifted to the left. GA activated the caspase-3 and 9 apoptotic pathway of SMMC-7721 cells to up-regulate the expression of pro-apoptotic protein Bax. Conclusion GA may induce the apoptosis of SMMC-7721 cells by mitochondrial apoptosis and inhibit the proliferation of SMMC-7721 cells.%目的 探讨没食子酸(gallic acid,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;Western blot检测相关蛋白表达.结果 GA作用SMMC-7721细胞48 h的IC50为(31.2±1.8)μg/mL;12.5、25、50μg/mL GA作用SMMC-7721细胞48 h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.