论文部分内容阅读
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。
OBJECTIVE: To investigate whether caspase (CAS) induced HO-8910 apoptosis in ovarian cancer involves reactive oxygen species generation and mitochondrial membrane depolarization. Methods: HO-8910 cells were cultured in vitro. Cell apoptosis rate was analyzed by AnnexinⅤ / PI double staining flow cytometry (FCM); H2DCFH-DA probe FCM was used to detect the production of reactive oxygen species; Rh123 probe FCM was used to analyze mitochondrial transmembrane potential. Results: CAS induced apoptosis in HO-8910 cells in a dose-dependent manner. CAS increased the level of ROS in HO-8910 cells in a concentration-dependent manner. The average fluorescence intensity of Rh123 in CAS-treated cells was significantly decreased, indicating that CAS had the effect of inducing mitochondrial membrane depolarization. N-acetyl-L-cysteine (NAC) partly antagonized CAS-induced apoptosis and attenuated CAS-induced ROS production and mitochondrial membrane depolarization. Conclusion: The mechanism of apoptosis induced by CAS in ovarian cancer HO-8910 cells may be related to the promotion of mitochondrial membrane depolarization induced by ROS production.