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作 者:谢晓东[1] 吴荧荧 黄文斯 刘庆[1] 王颖[1] 朱海涛[1] 张礼荣[1] 王冬青[1]
出 处:《江苏医药》2015年第6期624-626,F0002,共4页Jiangsu Medical Journal
基 金:江苏省自然基金(BK2011487);镇江市社会发展基金(SH2013026)
摘 要:目的探讨澳洲茄边碱(SM)对HepG2细胞增殖、凋亡的影响及其可能作用机制。方法用不同浓度SM 5、10、15和20μg/ml分别处理HepG2细胞3、6、12和24h,并设不加药的对照组。采用MTT法检测HepG2细胞增殖,DAPI染色法观察细胞核形态的变化,流式细胞术检测细胞凋亡和周期,Western blot法检测B细胞淋巴瘤-白血病2(Bcl-2)、Bcl相关X蛋白(Bax)、半胱天冬氨酸蛋白酶3(Caspase-3)及Ki67的蛋白表达。结果与对照组相比,SM呈剂量依赖性地抑制HepG2细胞增殖,促进HepG2细胞凋亡,将细胞周期阻滞于G2/M期,并且上调Bax和Caspase-3蛋白表达,下调Bcl-2和Ki67蛋白表达(P<0.05或P<0.01)。结论 SM能有效抑制HepG2细胞的增殖,促进细胞凋亡的发生;SM上调Bax和Caspase-3表达,下调Bcl-2和Ki67表达,细胞周期阻滞于G2/M期可能是其发挥上述作用的机制。Objective To investigate the effect and underlying mechanism of solamargine(SM)on the proliferation and apoptosis of HepG2 cells.Methods HepG2 cells were treated by different concentrations of SM 5,10,15 and 20μg/ml for 3,6,12 and 24hours,respectively.And SM 0μg/ml was taken as control group.The proliferation of HepG2 cells was determined by MTT method.The change of cell morphology was observed by DAPI staining.The cell apoptosis and cycle were measured by flow cytometry.The protein expressions of Bax,Bcl-2,Caspase-3and Ki67 were detected by Western blot.Results Compared with control group,SM inhibited cell proliferation in a concentrationdependent manner,promoted cell apoptosis,arrested cell cycle at G2/M phase,upregulated protein expressions of Bax and Caspase-3,and downregulated protein expressions of Bcl-2and Ki67(P〈0.05 or P〈0.01).Conclusion SM can effectively inhibit the proliferation of HepG2 cells and enhance cell apoptosis probably via upregulating Bax and Caspase-3expressions,downregulating Bcl-2and Ki67 expressions and arresting cell cycle at G2/M phase.
分 类 号:R329[医药卫生—人体解剖和组织胚胎学]
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