紫草素诱导人结肠癌细胞SW620凋亡及机制研究

目的探讨紫草素诱导人结肠癌细胞株SW620凋亡及分子机制。方法体外培养人结肠癌细胞株SW620,加入终浓度分别为2.5～15μmol/L的紫草素。采用MTT法测定紫草素对肿瘤细胞的增殖抑制率,Annexin V-FITC/PI双标法检测细胞凋亡率,Western blot方法测定对bcl-2、bax蛋白表达水平。结果紫草素随时间和浓度的增加对SW620细胞增殖抑制率增加,细胞凋亡率增加（P〈0.05）。Western blot法检测发现bax蛋白表达升高同时bcl-2蛋白表达下降。结论紫草素有抑制结肠癌细胞增殖和诱导凋亡的作用,可以通过调控bax和bcl-2蛋白的表达经线粒体途径诱导细胞凋亡。

Molecular Mechanism of Shikonion-induced Apoptosis of SW620 Cells

Objective To investigate the effects of Shikonion on apoptosis of human SW620 and explore the underlying molecular mechanism.Methods Human colon cancer cell SW620 was cultured in virto and treated with various concentrations（2.5-15 μmol/L） of Shikonion.Cell proliferation was examined by MTT assay and cell apoptosis were detected by Annexin V-FITC/PI double staining.The expression of bcl-2 and bax protein were detected by Western blot.Results Shikonion inhibited the growth of SW620 cells in a dose and time-dependent manner.SW620 cells treated with Shikonion for 24h showed significantly enhanced apoptosis as compared with control cells（P〈0.05）.Shikonion decreased bcl-2 and increased bax protein.Conclusion Shikonion may inhibit the proliferation and induce apoptosis of SW620 cells by changing the levels of bcl-2 and bax proteins.These findings indicated that depolarization of the mitochondrial membrane potential might be involved in Shikonion induced apoptosis.