摘要
探讨莱菔硫烷(SFN)通过线粒体途径诱导HepG-2细胞凋亡的机制.不同剂量SFN处理体外培养的HepG-2细胞株48h,流式细胞仪检测SFN对HepG-2细胞凋亡率影响;采用Western Blot法测定SFN对HepG-2细胞Cyt-c蛋白表达的影响;酶活性检测试剂盒测定SFN对HepG-2细胞内caspase-3和caspase-9酶活性的影响.SFN能够有效地诱导HepG-2细胞凋亡,10、20、40μmol/L的SFN作用于HepG-2细胞48h后,与对照组比较凋亡率显著升高(P<0.01),并呈剂量依赖性;SFN可使HepG-2细胞胞浆中Cyt-c蛋白含量升高,与对照组比较差异显著(P<0.05);同时使细胞内caspase-3和caspase-9的活性升高,并呈一定的剂量依赖性.SFN可诱导人肝癌HepG-2细胞的凋亡,可通过促进Cyt-c的释放,进而激活caspase-9,再激活下游caspase-3,最终引起细胞凋亡.
To investigate the mechanism of inducing apoptosis effect through the mitochondrial pathway in HepG-2 by sulforaphane （SFN）. HepG-2 cells are treated with different concentration of SFN in vitro for 48 hours. Flow cytometry is used to detect apoptosis rate of SFN on HepG-2,Western Blot is used to detect the expression of Cyt-c protein in HepG-2,and the activity detection kits are employed to examine the activity of caspase-3 and caspase-9. SFN could effectively induce cell apoptosis of HepG-2 and the apoptosis rates are increased in a dose-dependent manner（P0.01）. SFN could also remarkably up-regulate the expression of Cyt-c protein in HepG-2 cells （P0.05）. Meanwhile,the activity of caspase-3 and caspase-9 is increased which showed a dose-dependent manner. SFN can induce apoptosis of human hepatoma HepG-2 cells,and activating the mitochondrial apoptotic pathway is one of the main mechanism of SFN.
出处
《哈尔滨商业大学学报（自然科学版）》
CAS
2009年第6期641-644,共4页
Journal of Harbin University of Commerce：Natural Sciences Edition
基金
国家自然科学基金项目(30300284)
黑龙江省自然科学基金项目(D200802)
黑龙江省骨干教师项目(1154G36)
