人参皂甙Compound K对卵巢癌细胞增殖与凋亡的影响及其机制探讨

摘要

Objective To detect the influence of ginsenoside compound K (CK) on proliferation,apoptosis of SKOV3 cells.Methods Cell viabilities was analyzed by CCK8 assays.Cell cycle and apoptosis rate were detected by flow cytometry.Western-blotting assay was used to analyze the expression of apoptosis-related proteins.Results After treatment with 5 μmol/L CK for 48 h,the proliferation of SKOV3 cells was significantly inhibited,and the growth cycle was arrested in G0/G1 phase,the total apoptosis rate was 11.06％.The western blotting results showed that the expressions of mitochondrial-mediated apoptotic signaling pathway-related proteins such as anti-apoptotic protein Bcl-2 and Bcl-xl decreased,while the expression of pro-apoptotic protein Bid increased.However,the apoptotic signaling pathway mediated by death receptor (Fas/FasL) did not change significantly.Conclusion CK can significantly inhibit the proliferation of ovarian cancer cells and induce cell apoptosis via mitochondrial-mediated apoptotic pathway.%目的 探讨人参皂甙Compound K(CK)对人卵巢癌细胞株SKOV3细胞增殖以及凋亡的影响.方法 CCK-8法检测CK对卵巢癌SKOV3细胞增殖的影响;流式细胞术检测CK对细胞周期时相以及细胞凋亡的影响;免疫印迹法(western blotting)检测CK对凋亡信号通路相关蛋白表达的影响.结果 5μmol/L CK作用卵巢癌细胞48 h即可显著抑制细胞的增殖活性,细胞周期阻滞于G0/G 1期,总的细胞凋亡率为11.06％;Western blot检测结果提示,线粒体介导的细胞凋亡信号通路相关蛋白发生变化,如抗凋亡蛋白Bcl-2,Bcl-xl的表达随着药物剂量的增加而降低,而促凋亡蛋白Bid的表达随着药物剂量增加而升高;而死亡受体(Fas/FasL)介导的凋亡信号通路未见明显变化.结论 CK可显著抑制卵巢癌细胞的增殖活性,并通过线粒体介导的内源性凋亡通路诱导人卵巢癌细胞发生凋亡.