雷公藤内酯醇诱导非小细胞肺癌细胞凋亡及其机制初探

Apoptosis of Cancer Cells Inducing by Triptolide on Human Non-small Cell Lung Cancer in Vitro

目的:研究雷公藤内酯醇(Triptolide,TPL)对非小细胞肺癌细胞A549细胞增殖抑制作用和促凋亡影响的分子机制。方法:以A549细胞为研究对象,采用MTT法测定细胞增殖;吖啶橙/溴乙啶(AO/EB)荧光染色法检测细胞凋亡;Caspase3活性检测试剂盒分析其凋亡机制。结果:在6.25～100 ng·ml^(-1),12～72 h范围内,TPL对A549细胞增殖具有明显抑制作用(P<0.01),48 h内其凋亡率随着时间延长而增加,Caspase3活性早期较对照组有显著提高(P<0.05),并于12 h达到最高值。结论:TPL能有效抑制A549细胞的增殖,这种抑制作用可能与TPL促进肿瘤细胞凋亡,激活Caspase3活性有关。

Objective： To investigate the effects of proliferation inhibitory and the molecule mechanism of apoptosis induced by triptolide on A549 cells. Method： Non-small cell lung cancer cell line A549 was used. The effects of triptolide on cell proliferation were observed by MTT method in vitro. The apoptosis was evaluated by AO/EB fluorescent staining and caspase-3 fluorometric assay kit. Result： Triptolide exhibited a marked antiproliferative effect on A549 cells within the concentration from 6.25 to 100 ng·ml^-1 and the time from 12 to 72 hours（P 〈 0.01 ）. The apoptotic ratio was time-dependant in 48 hours （P 〈 0.01 ）. The activity of Caspase-3 had a significant increase compared to the control group（P 〈 0.05） in early times and reached a maximum after 12 hours. Conclusion： Triptolide can inhibit the proliferation on A549 cell effectively. The effect may be correlated with the apoptosis-inducing activity and the Caspase-3 activation from triptolide.