文献类型：期刊文献

中文题名：血根碱通过诱导活性氧促进HepG2细胞凋亡的机制研究

英文题名：Sanguinarine promotes apoptosis of HepG2 cells by inducing ROS

作者：杨艺萱[1];郭文静[2];马承旭[2];苏海燕[1];宋鹏[1,3]

第一作者：杨艺萱

机构：[1]甘肃中医药大学附属医院检验科;[2]甘肃中医药大学临床医学院;[3]甘肃省中医药防治慢性疾病重点实验室,甘肃兰州730000

第一机构：甘肃中医药大学第二附属医院

年份：2018

卷号：34

期号：3

起止页码：370

中文期刊名：中国药理学通报

外文期刊名：Chinese Pharmacological Bulletin

收录：CSTPCD;;Scopus;北大核心:【北大核心2017】；CSCD:【CSCD2017_2018】；

基金：甘肃省卫生行业科研计划管理项目(No GWGL2014-53);甘肃省中医药防治慢性疾病重点实验室开放课题(No GSMBKY2015-01)

语种：中文

中文关键词：血根碱;HepG2细胞;活性氧;凋亡;肝癌;信号通路

外文关键词：sanguinarine;HepG2 cells;ROS;apoptosis;hepatic carcinoma;signaling pathway

摘要：目的研究血根碱对Hep G2细胞中活性氧(ROS)调控细胞凋亡途径的影响。方法采用血根碱干预Hep G2细胞,MTT法检测血根碱对细胞活性的影响;DCFH-DA和DHE染色观察血根碱作用Hep G2细胞12 h后细胞内ROS的变化;Hoechst 33342和Annexin V/PI染色检测细胞凋亡;Rho123染色检测细胞线粒体膜电位;Western blot检测凋亡相关蛋白的表达。结果随着血根碱药物浓度的增加,Hep G2细胞活力明显被抑制;血根碱可以明显提高Hep G2细胞内的ROS含量,并且降低线粒体膜电位,促进细胞凋亡;Western blot检测发现血根碱促进Bax、cleaved-caspase-3和细胞质Cyt-C的表达,抑制Bcl-2蛋白的表达。结论血根碱通过升高细胞内ROS的含量,激活线粒体凋亡途径,进而促进Hep G2细胞发生凋亡。
Aim To investigate the effect of sanguinarine on regulating the pathway of cell apoptosis by inducing reactive oxygen species（ ROS） in Hep G2 cells. Methods MTT method was used to detect the cell viability of Hep G2 cell after the treatment of sanguinarine. The changes of ROS were observed by indicator DCFH-DA and DHE staining. The apoptosis was detected by Hoechst 33342 and Annexin V/PI staining; Rhodamine 123 staining was used to detect mitochondrial membrane potential. Western blot was used to detect expressions of key cell-apoptotic protein. Results The cell viability of Hep G2 cells showed a decreasing trend with the increasing concentration of sanguinarine. Sanguinarine could significantly increase cellular ROS,decrease mitochondrial membrane potential in Hep G2 cell,and promote apoptosis of Hep G2 cells. The expression of Bax,cleaved-caspase-3 and cytoplasmic Cyt-C significantly increased after the treatment of sanguinarine,however,the expression of Bcl-2 was inhibited. Conclusion Sanguinarine could activate mitochondrial pathway of apoptosis mediated by cellular uncontrolled ROS and promote apoptosis of Hep G2 cells.