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机构地区:[1]哈尔滨医科大学公共卫生学院营养与食品卫生学教研室,黑龙江哈尔滨150081
出 处:《癌变.畸变.突变》2007年第2期99-102,共4页Carcinogenesis,Teratogenesis & Mutagenesis
基 金:国家自然科学基金项目(30371227);哈尔滨医科大学研究生创新基金资助
摘 要:背景与目的:探讨Bax蛋白在维生素E琥珀酸酯(vitamin E succinate,VES)诱导人胃癌SGC-7901细胞凋亡中的作用。材料与方法:用吖啶橙/溴化乙啶(AO/EB)染色观察细胞凋亡的形态学改变;Western Blot法检测不同剂量VES对人胃癌SGC-7901细胞中Bax蛋白表达量的影响和VES对Bax蛋白与细胞色素c(cytochrome c,Cyt c)蛋白在细胞内分布的影响;用Mito Tracker Red CMXRos荧光染色观察线粒体膜电位(ΔΨm)的变化。结果:VES可引起SGC-7901细胞发生凋亡,提高Bax蛋白表达水平,并使Bax蛋白从胞浆转移到线粒体;VES作用后发生线粒体膜电位下降,Cyt c从线粒体释放到胞浆。结论:VES可能通过Bax蛋白来启动线粒体凋亡途径,诱导SGC-7901细胞发生凋亡。BACKGROUND & AIM: To study the possible effect of Bax in vitamin E succinate-induced apoptosis of human gastric carcinoma. MATERIALS AND METHODS: Fluorescent staining was used to detect apoptosis and the mitochondrial transmembrane potential(ΔΨm) of human gastric carcinoma SGC-7901 cells. The expression of Bax was measured by Western Blot analysis after the cells were treated with VES at 5, 10, 20μg/ml. The translocation of Bax and cytochrome c were determined by Western Blot analysis in mitochondrial and cytosolic-enriched cellular fractions. RESULTS: VES caused apoptosis of SGC-7901 cells. The expression of Bax was increased in whole cell lysate with a dose-dependent relationship. Bax was translocated from the cytosol to the mitochondria. The permeabilization of rnitochondrial membranes was increased as determined by the loss of ΔΨm. And cytochrome c was released from the mitochondria to the cytosol. CONCLUSION: VES could induce apoptosis of human gastric carcinoma SGC-7901 cells through mitochondrial pathway by Bax.
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