吉西他滨对人肝癌HepG2细胞增殖和凋亡影响的实验研究  

The effect of gemcitabine cell proliferation and apoptosis of of human hepatocellular carcinoma HepG2 cell

作　　者：李毅[1] 田涛[1] 袁张莉[1] 姚煜[1] 南克俊[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：《现代肿瘤医学》2010年第12期2329-2332,共4页Journal of Modern Oncology

摘　　要：目的:探讨吉西他滨对肝癌HepG2细胞株增殖和凋亡的影响及其可能的分子机制。方法:MTT法测定吉西他滨不同浓度和时间作用后肝癌HepG2细胞的增殖抑制率;流式细胞仪检测吉西他滨作用HepG2细胞后细胞周期分布及凋亡情况;免疫细胞化学法、Western blot法分别检测吉西他滨作用后细胞凋亡相关因子Survivin及Bcl-2的表达。结果:在0.3715-5mg/L浓度范围内,吉西他滨对HepG2的生长具有明显的抑制作用,并呈时间和剂量依赖性;0.3715mg/L的吉西他滨可导致HepG2细胞G0/G1期阻滞,并引起细胞凋亡;免疫细胞化学和Western blot的结果显示吉西他滨作用后Survivin和Bcl-2的表达下调。结论:吉西他滨可抑制HepG2细胞增殖并诱导凋亡,其诱导凋亡的机制与Survivin和Bcl-2的表达下调有关。Objective：To investigate the effect of gemcitabine（GEM） on cell proliferation and apoptosis of on hepatocellular carcinoma HepG2 cell line and the molecular mechanism.Methods：The cell proliferation inhibition of HepG2 cells by GEM was observed by MTT assay.The cell cycle and apoptosis of HepG2 cells exposed to GEM was analyzed by flow cytometry.The expressions of survivin and Bcl-2 after GEM treatment were examined by immunocytochemical and Western blot method.Results：Within 0.3715-5 mg/L,GEM obviously inhibited the proliferation of HepG2 cells in a time-and dose-dependent manner.0.3715 mg/L GEM caused HepG2 cells to undergo G0/G1 arrest and induced apoptosis.Immunohistochemical method and Western blot method showed that the expression of Survivin and Bcl-2 were decreased after GEM treatment.Conclusion：GEM can obviously inhibit HepG2 cell proliferation and induce cell apoptosis.The mechanism of this apoptotic effect is closely related to downregulation of expression of survivin and Bcl-2.

关 键 词：肝癌 吉西他滨 SURVIVIN BCL-2 

分 类 号：R735.7[医药卫生—肿瘤]