表没食子儿茶素没食子酸酯通过PI3K/AKT信号通路抑制人肝癌细胞株HepG2增殖和促进凋亡  

Epigallocatechin-3-gallate induces human liver cancer HepG2 cell apoptosis and growth inhibition by suppressing phosphatidylinositol3 kinase/protein kinase B signaling

作　　者：李懿[1] 赵莉莉[2] 李易[1] 赵燕[3] 李良平[1] 

机构地区：[1]四川省人民医院消化内科,四川省成都市610072 [2]北京大学人民医院消化内科,北京市100044 [3]国家体育总局运动医学重点实验室运动医学四川省重点实验室,四川省成都市610072

出　　处：《世界华人消化杂志》2015年第20期3188-3194,共7页World Chinese Journal of Digestology

摘　　要：目的:探讨表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG),对人肝癌细胞株HepG2的作用及其机制.方法:对数生长期的HepG2细胞分别用不同浓度的EGCG处理(0、10、20、40冚g/mL).细胞培养48 h后,利用MTT检测细胞增殖;流式检测细胞凋亡和膜电位,免疫印迹法检测磷脂酰肌醇-3-激酶(phosphatidylinositol3 kinase,PI3K)、蛋白激酶B(protein kinase B,AKT)、p-AKT、BCL-2、Bax、proCaspase3、clevage-Caspase3、多聚ADP-核糖聚合酶[poly(ADP-ribose)polyrnerase,PARP]、Clevage-PARP和细胞色素C(cytochrome C,CytC)表达.结果:EGCG可以成浓度依赖诱导HepG2细胞增殖抑制和凋亡,上调Bax,pro-Caspase3,PARP和CytC表达,下调PI3K,p-AKT,Cleavage-PARP,Cleavage-Caspase3和Bcl-2的表达和细胞膜电位,但对AKT表达无明显影响.结论:EGCG可通过抑制PI3K/AKT信号通路而诱导HepG2细胞增殖抑制和凋亡.AIM： To investigate the effect of epigallocatechin- 3-gallate （EGCG） on cell apoptosis and prolifera- tion in the human liver cancer cell line HepG2 and to explore the underlying mechanism. METHODS： HepG2 cells in logarithmic growth phase were treated with different concentrations of EGCG （（3, 10, 20, 40 μg/mL） for 48 h. MTT and flow cytometric analysis were used to evaluate the proliferation, membrane potential and apoptosis of HepG2 cells. The expression of phosphatidylinositol 3 kinase （PI3K）, p-protein gase B （p-AKT）, AKT, BCL-2, Bax, pro-Caspas3, cleaved Caspase3, poly（ADP-ribose） polymerase （PARP）, cleaved PARP and cytochrome C （CytC） in HepG2 cells was detected by Western blot. RE SU LTS： EGCG treatment significantly decreased the cell proliferation, membrane potential and the expression of PI3K, p-AKT, cleaved PARP, cleaved Caspase3 and Bcl-2 in HepG2 cells, and increased cell apoptosis and the expression of pro-Caspase3, PARP, CytC and Bax. However, EGCG treatment had no significant influence on the expression of AKT. CONCLUSION： EGCG induces cell apoptosis and growth inhibition in the human liver cancer cell line HepG2 possibly, by suppressing PI3K/ AKT signaling

关 键 词：表没食子儿茶素没食子酸酯 HEPG2 增殖 凋亡 PI3K/AKT 

分 类 号：R735.7[医药卫生—肿瘤]