亚硒酸钠诱导K562细胞凋亡作用及机制探讨

Research on the mechanism of sodium selenite inducing K562 cells apoptosis

目的:探讨亚硒酸钠诱导K562细胞凋亡的作用及机制。方法:不同浓度亚硒酸钠作用K562细胞后,MTT法检测细胞增殖抑制,电镜和TUNEL法检测K562细胞的凋亡,RT-PCR检测Bcl-2和Bax的mRNA表达变化,分光光度法检测Caspase-3的活性变化。结果:亚硒酸钠能抑制K562细胞的生长增殖,诱导其凋亡。20μmol/L亚硒酸钠作用K562细胞48h后,Bcl-2表达明显降低,Bax表达明显升高,Caspase-3活性升高,与对照组相比具有显著的统计学意义(P<0.01)。结论:亚硒酸钠能够诱导K562细胞凋亡,其机制可能与下调Bcl-2,上调Bax,活化Caspase-3有关。

Objective：To investigate the effects of sodium selenite on the cell apoptosis of K562 ceils and to elucidate its molecular mechanisms. Methods： K562 cells were treated with various concentrations of sodium selenite at different time points, and then MTT assay was employed to evaluate the effects of sodium selenite on the proliferative inhibition of K562 cells.MTT assay was employed to evaluate the effects of sodium selenite on the proliferative inhibition of K562 cells. Electronmicroscopy, and TUNEL were performed to confirm the apoptosis of K562 cells,RT-PCR was employed to analyze the mRNA expression levels of Bcl-2 and Bax. Colorimetric method were used to measure the activities of caspase-3 of K562. Results：Sodium selenite could inhibit proliferation of K562 cells and induce them to undergo apoptosis. RT-PCR results showed that sodium selenite could decrease the mRNA expression level of Bcl-2 and increase the level of Bax of K562 ceils which had been treated with sodium selenite for 48h significantly, and the activity of caspase-3 elevated remarkably too. Compared with the control group, the expression levels of Bcl-2, Bax and acivity of caspase-3 in 20μmol/L sodium selenite treatment group were markedly changed（P〈0.05）. Conclusions：Sodium selenite can induce K562 ceils to undergo apoptosis. The decrease of mRNA expression level of Bcl-2, the increase of Bax and activity of caspase-3 may be its mechanisms.