得力生对肝癌HepG2细胞株凋亡的影响及机制  

Effect of Delisheng on apoptosis of liver cancer HepG2 cell line and its mechanism

作　　者：姚煜[1] 海亚楠[1] 南克俊[1] 袁张莉[1] 聂艳丽[1] 

机构地区：[1]西安交通大学医学院第一附属医院肿瘤内科,陕西西安710061

出　　处：《第四军医大学学报》2009年第18期1725-1727,共3页Journal of the Fourth Military Medical University

摘　　要：目的:探讨中药得力生对肝癌HepG2细胞株凋亡率的影响及可能的分子机制.方法:以MTT法检测不同浓度得力生作用不同时间后肝癌HepG2细胞的增殖抑制率的变化,用流式细胞仪检测细胞周期及凋亡,用免疫细胞化学法、Western Blot法分别观察细胞凋亡相关因子Caspase-3,Caspase-9及Bcl-2(B细胞淋巴瘤2)的表达.结果:得力生对肝癌HepG2细胞株的增殖抑制作用随药物作用时间和浓度增大而增加;主要使HepG2细胞株阻滞于S期;与对照组比较,实验组细胞凋亡率增高(P<0.01);Caspase-3和Caspase-9在实验组表达增加,Bcl-2表达减少.结论:得力生可以增加HepG2细胞株凋亡率,其作用机制可能与线粒体凋亡通路有关.AIM： To investigate the effect of Delisheng on the apoptosis of hepatocellular carcinoma HepG2 cell line and to explore the molecular mechanism. METHODS： The inhibitory effect of Delisheng on HepG2 cell line＇s proliferation in vitro was assessed by MTT assay. The cell line cycle changes and the apoptotic rate of the treated cell were detected by flow cytometry and the expressions of Caspase-3, Caspase-9 and Bel-2 （ B cell lymphoma 2） were examined by immunocytochemical method and Western blot. RESULTS： Delisheng＇s effect on the proliferation of HepG2 cell line increased with the increasing drug dose and drug action time. Delisheng caused cell cycle arrest at S phase and significantly increased the apoptosis rate of the HepG2 cell line. The expressions of both Caspase-3 and Caspase-9 increased while Bcl-2 decreased, compared with those in blank group. CONCLUSION： Delisheng obviously increases HepG2 cell line＇s apoptotic rate and this apoptotic effect may relate to the mitochondrial apoptosis pathway.

关 键 词：肝癌 得力生 CASPASE-3 CASPASE-9 BCL-2 

分 类 号：R735.7[医药卫生—肿瘤]