紫花牡荆素体外抑制人卵巢癌HO-8910细胞增殖和诱导凋亡的研究

Effect of casticin on inhibition of proliferation and induction of apoptosis of human ovarian cancer HO-8910 cells in vitro

目的:探讨紫花牡荆素(casticin)体外抑制人卵巢癌HO-8910细胞增殖和诱导凋亡的效应及其机制。方法:MTT法检测casticin对人卵巢癌HO-8910细胞增殖的抑制;Hoechest33258染色观察细胞凋亡形态学改变;流式细胞术(FCM)检测casticin处理HO-8910细胞的凋亡率;Western blotting分析caspase-3、CyclinB1、p21蛋白表达变化。结果:casticin对人卵巢癌HO-8910细胞增殖有较强的抑制作用,呈剂量和时间依赖性。经casticin作用48h后HO-8910细胞表现出典型的凋亡形态特征,并剂量依赖性地增加亚二倍峰,降低CyclinB1蛋白表达,增高caspase-3和p21表达。结论:casticin通过降低CyclinB1表达、活化p21和caspase-3抑制HO-8910细胞增殖并诱导凋亡。

Objective：To investigate the effect of casticin on inhibition of proliferation and apoptosis of human ovarian cancer HO-8910 cells in vitro.Methods：The inhibitory effect of casticin on the proliferation of human ovarian cancer HO-8910 cells was evaluated by the MTT assay and the apoptotic effect was demonstrated by Hoechst 33258 staining and flow cytometric analysis.The expressions of caspase-3,Cyclin B1,p21 were analyzed by Western blotting.Results：Casticin significantly inhibited the proliferation of human ovarian cancer HO-8910 cells in a dose-dependent and time-dependent manner,and the IC50 was 6.46 μg/ml for 48hours.The cells treated with casticin showed typical morphological change of apoptosis and increased cells of sub-G1 population by the flow cytometric analysis in a dose-dependent.Western blotting showed that expressions of caspase-3 protein and p21 protein were upregulated and protein level of Cyclin B1 was depressed after treatment with casticin in a concentration dependent.Conclusion：Casticin can inhibit proliferation and induce apoptosis of human ovarian cancer HO-8910 cells in vitro through downregulation of Cyclin B1 expression and activation of p21 and caspase-3.