淫羊藿苷对人卵巢癌细胞株的肿瘤恶性行为的抑制作用研究

The Roles of Icariin on the Proliferation and Apoptosis Abilities of Human Oophoroma Cells and Multi-drug Resistant Cell Line

目的探讨淫羊藿苷对人卵巢癌细胞SKOV3及多药耐药细胞株SKVCR增殖、凋亡、侵袭和迁移的影响。方法以不同质量浓度淫羊藿苷溶液分别作用于SKOV3细胞和SKVCR细胞,CCK8实验检测其抑制率及半数抑制浓度(IC50);并以0.8倍IC50质量浓度淫羊藿苷处理细胞,流式细胞仪检测对细胞增殖和凋亡的影响;Transwell实验检测细胞迁移和侵袭能力,免疫印迹法检测Caspase-3蛋白表达水平。结果淫羊藿苷抑制SKOV3及SKVCR细胞增殖,且在5~100μg/mL质量浓度范围内呈量效正相关趋势;淫羊藿苷分别以19.5μg/mL和48.4μg/mL(0.8倍IC50)质量浓度作用于SKOV3细胞及SKVCR细胞后,SKOV3及SKVCR细胞凋亡率均较对照组增加(P<0.05);同时,与对照组相比,细胞增殖、迁移和侵袭能力均下降(P<0.05),免疫印迹结果显示,淫羊藿苷可增加卵巢癌细胞Caspase-3蛋白表达(P<0.05)。结论淫羊藿苷能抑制人卵巢癌细胞SKOV3及多药耐药细胞株的增殖、迁移和侵袭能力,并上调Caspase-3蛋白表达,诱导细胞凋亡。

Objective To explore the effects of icariin on the proliferation and apoptosis abilities of human ovarian cancer cells SKOV3 and multi-drug resistant SKVCR cells.Methods Human ovarian cancer cells SKOV3 and multi-drug resistant SKVCR cells were treated with various concentrations of icariin. The inhibitory concentration and the half maximal inhibitory concentration were detected by CCK8 kit.The proliferation and apoptosis abilities of SKOV3 and SKVCR cells were measured by flow cytometry.The migration and invasion abilities of SKOV3 and SKVCR cells were evaluated by Transwell assays.The protein expression level of Caspase-3 was detected by Western blot analysis.Results Icariin significantly suppressed the proliferation abilities of SKOV3 and SKVCR cells in a dose-dependent manner at variant levels from 5-100μg/mL.SKOV3 and SKVCR cells were treated with 19.5μg/mL icariin and 48.4μg/mL icariin（0.8×IC50）for 48 h,respectively.The results showed that the cell proliferation,migration and invasion abilities were markedly decreased comparing with control group,and the apoptosis rate was significantly increased as compared with control group（P〈0.05）.Western blot results indicated that icariin significantly increased the protein expression level of caspase-3 in SKOV3 and SKVCR cells（P〈0.05）.Conclusion Icariin suppressed the proliferation,migration and invasion abilities of human ovarian cancer cells.Increasing expression of Caspase-3 might be the mechanism of its enhancement of apoptosis.