活性氧介导紫花牡荆素诱导卵巢癌HO-8910细胞调亡

目的:探讨紫花牡荆素(Casticin,CAS)诱导人卵巢癌HO-8910细胞凋亡是否涉及活性氧生成和线粒体膜去极化。方法:体外培养HO-8910细胞。AnnexinⅤ/PI双染色流式细胞术(FCM)分析细胞凋亡率;H2DCFH-DA探针FCM检测细胞活性氧生成;Rh123探针FCM分析细胞线粒体跨膜电位。结果:CAS诱导HO-8910细胞凋亡率增高,呈剂量依赖性。CAS以浓度依赖方式增高HO-8910细胞内活性氧水平。CAS处理细胞的Rh123平均荧光强度显著降低,表明CAS具有诱导细胞线粒体膜去极化作用。N-乙酰半胱氨酸(N-acetyl-L-cysteine,NAC)部分拮抗CAS诱导细胞凋亡,并能减弱CAS诱导活性氧生成和线粒体膜去极化作用。结论:CAS诱导卵巢癌HO-8910细胞凋亡作用机制可能与促进细胞活性氧生成介导的线粒体膜去极化相关。

Reactive oxygen species mediated induction of apoptosis by casticin in ovarian cancer HO-8910 cells

Objective To investigate whether casticin-induced apoptosis in ovarian cancer HO-8910 cells is involved in reactive oxygen species-mediated mitochondrial membrane depolarization.Methods Human ovarian cancer HO-8910 cells were cultured in vitro.The apoptotic rate was analyzed by flow cytometry(FCM) with Annexin V/PI double staining.Intracellular reactive oxygen species(ROS) was measured by FCM with fluorescent probe 2’,7’-dichlorodihydrofluorescein diacetate(H2DCFH-DA).The FCM with rhodamine 123 was used to analyze the mitochondrial transmembrane potential.Results CAS induced apoptosis of HO-8910 ovarian cancer cells in a time-dependent manner.CAS significantly elevated ROS level in HO-8910 cells,in a concentration-dependent manner.The average intracellular fluorescence intensity of rhodamine 123 in cells treated with CAS was significantly reduced,indicating that CAS induced mitochondrial membrane depolarization.N-acetyl-L-cysteine(NAC) attenuated induction of apoptosis,ROS generation,and mitochondrial membrane depolarization by CAS in HO-8910 cells.Conclusion CAS-induced apoptosis of human ovarian cancer HO-8910 cells may be associated with ROS generation and mitochondrial membrane depolarization.