Genistein对卵巢癌铂类耐药细胞株CP70增殖凋亡的影响及与细胞内ROS的相关性

目的:探讨Genistein对卵巢癌铂类耐药细胞CP70增殖、凋亡的影响及与细胞内活性氧水平的关系。方法:采用MTT法检测Genistein对CP70细胞增殖的影响;流式细胞仪分析不同药物处理后对细胞凋亡的影响,线粒体膜电位及细胞内ROS水平的变化情况。结果:Genistein对CP70细胞增殖表现出剂量和时间依赖性的抑制作用,并能诱导其凋亡;Genistein作用于CP70细胞后,可使其线粒体膜电位降低,并引发了细胞内ROS水平的显著升高;ROS抑制剂NAC预处理CP70细胞后,有效抑制了ROS的产生,并降低了细胞凋亡率,与未加NAC组相比差异有显著性(P0.05)。结论:Genistein能抑制铂类耐药卵巢癌细胞CP70的增殖,并促进其凋亡,这与细胞内ROS水平的升高有关,可能是Genistein抗肿瘤诱导细胞凋亡的机制之一。

Effects of Genistein on Proliferation, Apoptosis and the Level of ROS in Human Ovarian Carcinoma Cell CP70

Objective： To investigate the effects of Genistein on proliferation, apoptosis and the level of ROS in drug resistant Human Ovarian Carcinoma Cell CP70. Methods： The growth inhibitory effect of different drugs on CP70 cells was detected by MTT assay. The apoptosis rate was determined by flow cytometry. Mitochondrial membrane potential and the level of ROS were measured by flow cytometry. Results： The exerted inhibitory effect of Genistein on CP70 cells in a time and dose dependent manner, and it could induce the apoptosis of CP70 cells. Genistein reduced the mitochondrial membrane potential and increased the level of ROS. After pretreatment with antioxidant NAC, the level of ROS was effectively inhibited, meanwhile mitochondrial membranee potential increased and apoptotic rate decreased. Conclusion： Genistein inhibited the proliferation and induced apoptosis, and is related to the increased of ROS in cisplatin-resistant ovarian cancer cell CP70. It may be one of the mechanism of apoptosis induced by Genistein in CP70 cells.