2-甲氧基雌二醇诱导K562细胞凋亡的机制研究

目的探讨2-甲氧基雌二醇(2-ME)对K562细胞的凋亡诱导效应及其作用机制。方法使用不同浓度2-ME(0,5,10,20,40μmol/L)作用于K562细胞,48 h后用流式细胞术检测2-ME作用后K562细胞的凋亡率的变化;用western blot方法检测2-ME作用48 h后K562细胞Bcl-2、Bax和Caspase-3蛋白的表达。结果 (1)2-ME在5~40μmol/L浓度范围内作用48 h对K562细胞有凋亡诱导作用,与对照组比较差异有显著性(P<0.05),这种作用呈剂量依赖关系;(2)2-ME作用48 h后,K562细胞Bcl-2蛋白的表达较对照组减少,差异有显著性(P<0.05),而Bax和Caspase-3表达较对照组增高,差异有显著性(P<0.05)。结论 2-ME可能通过线粒体途径诱导K562白血病细胞凋亡。

Mechanism research on apoptosis of K562 cells induced by 2-methoxyestradiol

Objective To investigate mechanism of apoptosis of K562 cells induced by 2-methoxyestradiol(2-ME).Methods K562 cells were treated with 2-ME(0,5,10,20,40 μmol/L) for 48 h.The cell apoptosis was measured by flow cytometry.Expressions of Bcl-2,Bax and Caspase-3 proteins in K562 cells were detected by western blot.Results(1) 2-ME with various concentrations(0,5,10,20,40 μmol/L) could induce the cell apoptosis of K562 cells,and the apoptosis rate of K562 cells significantly increased(P<0.05) in a dose-dependent manner.(2) Bcl-2 protein expression decreased significantly in 2-ME treated group compared with the control group(P<0.05),while Bax and Caspase-3 protein expressions were elevated significantly in 2-ME treated group compared with the control group(P<0.05).Conclusion The apoptosis of K562 cells induced by 2-methoxyestradiol might associated with the mitochondrial pathway.