中文摘要：

目的探讨甘草酸苷对肝癌细胞SMCC-7721凋亡诱导作用及相关机制。方法以甘草酸苷（0、10、30、100μg/mL）处理肝癌细胞SMCC-7721 48h后,咪唑蓝（MTT）法检测肝癌细胞活力的影响;流式细胞术检测细胞凋亡和线粒体膜电位;紫外分光光度法检测细胞中含半胱氨酸的天冬氨酸蛋白水解酶3（Caspase-3）、Caspase-9活性的影响;Western blot分析线粒体途径中相关蛋白p53、细胞色素C（CytC）、B淋巴细胞瘤-2（Bcl-2）和Bcl-2相关蛋白（Bax）的表达。结果与阴性对照比较,10、30、100μg/mL甘草酸苷可显著降低细胞的活力（P〈0.01）,诱导细胞凋亡（P〈0.01）,促进线粒体膜电位去极化（P〈0.01）,抑制肝癌细胞SMCC-7721Caspase-3、Caspase-9活性（P〈0.01）,并上调p53、CytC、Bax的表达（P〈0.01）,下调Bcl-2的表达（P〈0.01）,且作用呈现浓度依赖关系。结论甘草酸苷可通过线粒体途径诱导肝癌细胞SMCC-7721凋亡。

英文摘要：

Objective To explore the molecular biological mechanism and induction of glycyrrhizin on apoptosis in hepatocellular carcinoma cell SMCC-7721.Methods MTT method was used to detect the viability of SMCC-7721 cells after the cells were cultured with glycyrrhizin of 0（negative control）,10,30 and 100μg/mL.The mitochondrial membrane potential and cell apoptosis of SMCC-7721 cell was measured by flow cytometry.The activity of Caspase-3,Caspase-9was assayed by spectrophotometric assay.The mitochondrial pathway related protein p53,cytochrome（CytC）,Bax,Bcl-2was assayed by Western blot.Results Compared with negative control group,10,30,100μg/mL glycyrrhizin inhibited SMCC-7721 cell viability（P〈0.01）,induced SMCC-7721 cell apoptosis and promoted mitochondrial membrane potential depolarization（P〈0.01）,as well as inhibited the activity of Caspase-3and Caspase-9（P〈0.01）,upregulated the expression of p53,CytC,Bax（P〈0.01）and down-regulated the expression of Bcl-2（P〈0.01）.The effects were related with the medicine concentration in does-dependent.Conclusion glycyrrhizin could induce SMCC-7721 cell apoptosis,which might be related with mitochondrial pathway.