论文部分内容阅读
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 and mechanism of casticin on proliferation and apoptosis of HO-8910 human ovarian cancer cells in vitro. Methods: The inhibitory effect of casticin on the proliferation of HO-8910 cells was detected by MTT assay. The morphological changes of apoptosis were observed by Hoechest33258 staining. The apoptosis rate of HO-8910 cells treated by casticin was detected by flow cytometry (FCM) Caspase-3, CyclinB1, p21 protein expression changes. RESULTS: casticin had a strong inhibitory effect on the proliferation of HO-8910 human ovarian cancer cells in a dose and time-dependent manner. After 48 hours treatment with casticin, HO-8910 cells showed typical morphological features of apoptosis and increased dose-dependently sub-doubling peak, decreasing the expression of CyclinB1 protein and increasing the expression of caspase-3 and p21. CONCLUSION: Casticin can inhibit HO-8910 cell proliferation and induce apoptosis by decreasing the expression of CyclinB1, activating p21 and caspase-3.