期刊论文

中文

中国现代医药杂志

1672-9463

2010

12

2

12-15

10.3969/j.issn.1672-9463.2010.02.004

湖南省衡阳市科技局资助项目（编号:2008KJ008）；

本校为第一机构

目的研究三氧化二砷（arsenic trioxide,As2O3）诱导HepG2细胞凋亡及其机制。方法采用MTT法、形态学观察及流式细胞术方法检测As2O3对HepG2细胞的生长抑制、凋亡作用的影响,用Western blot检测As2O3处理后HepG2细胞内凋亡相关蛋白Bcl-2和caspase-3的表达。结果As2O3对HepG2细胞有明显的抑制增殖作用,且呈浓度和时间依赖性,细胞呈典型的凋亡形态学改变,As2O3呈时间依赖性诱导HepG2细胞凋亡。As2O3处理不同时间后,Bcl-2蛋白表达水平下调,caspase-3蛋白表达水平升高。结论As2O3具有诱导人肝癌HepG2细胞凋亡的作用,其机制可能与其下调Bcl-2蛋白的表达,促进caspase-3活化有关。

Objective To investigate the apoptosis in human hepatocarcinoma HepG2 cells induced by As2O3 and study the mechanism.Methods MTT assay,morphology and flow cytometry were used to detect the inhibitory effect of arsenic trioxide （As2O3） on the growth of HepG2 cells and its inducing effect on the apoptosis of HepG2 cells.The expression of apoptosis-related proteins Bcl-2 and caspase-3 of HepG2 cells were estimated by western blot.Results MTT assay showed that As2O3 clearly inhibited growth of HepG2 cells,which depending time and dosage.The typic...