二氢青蒿素抑制结肠癌细胞株HCT-116并诱导凋亡的实验研究

目的：研究二氢青蒿素（Dihydroartemisinin,DHA）对人结肠癌HCT-116细胞的体外抑制并诱导凋亡,并探讨其作用机制。方法：以不同浓度的DHA作用于体外培养的HCT-116细胞,采用四甲基偶氮唑盐比色法（MTT法）检测细胞生长抑制率;应用流式细胞仪进行周期分析检测细胞凋亡情况;用Western Blotting法,检测不同浓度的DHA作用于肿瘤细胞时,凋亡相关蛋白Bcl-2,bax,cleavad-PARP表达情况。结果：在DHA作用后,HCT-116细胞生长受到明显抑制,IC50（半抑制浓度）值为14.18μmol/L。并呈一定的量效和时效依赖关系。流式细胞仪检测亚二倍体（sub-G0）比例增高;Western-Blotting检测药物处理细胞后Bcl-2表达水平下调,而Bax、cleavad-PARP表达水平明显上调。结论：DHA能抑制HCT-116细胞的生长增殖并诱导细胞发生凋亡。

Effect of Dihydroartemisinin on Apoptosis and Cell Growth Inhibitory in Human Colon Cancer HCT-116 Cells

Objective：To investigate the effect of dihydroartmisinin on apoptosis and cell growth inhibitory in Human Colon cancer Hct116 cells cultured in vitro.Methods：HCT-116 cells were treated with DHA at various concentrations and determined for proliferation inhibiting rate by MTT method.The apoptosis induction was examined by flow cytometry.The expression of the Bcl-2,bax,cleavad-PARP which associated with cell apoptosis were measured by Western-Blotting.Results：DHA showed significantly time-and dosage-dependent inhibitouy effect on the proliferation of HCT-116 cells,the IC50 values were 14.18 μmol/L.Flow cytometry demonstrated that the percentage of the cells in Sub-G0 phase increase remarkably after treated with DHA.Western-Blotting also revealed that DHA down-regulated Bcl-2,up-regulated Bax and cleavad-PARP.Conclusions：DHA can induce apoptosis and inhibit the proliferation of HCT-116 cells significantly.