Bcl-2家族蛋白在维生素E琥珀酸酯诱导人胃癌细胞凋亡中的作用  

THE ROLE OF BCL-2 FAMILY PROTEIN IN VITAMIN E SUCCINATE INDUCED APOPTOSIS OF HUMAN GASTRIC CANCER CELL LINES

作　　者：张晓华[1] 苑林宏[1] 单毓娟[1] 张岭[1] 吴坤[1] 

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,哈尔滨150081

出　　处：《营养学报》2007年第1期31-34,共4页Acta Nutrimenta Sinica

基　　金：国家自然科学基金(No.30371227);哈尔滨医科大学研究生创新基金

摘　　要：目的:研究Bcl-2家族蛋白在维生素E琥珀酸酯(RRR-α-tocopheryl succinate,α-TOS;vitamin E succinate,VES)诱导人胃癌SGC-7901细胞凋亡线粒体途径中的作用。方法:采用噻唑蓝(MTT)法测定VES对SGC-7901细胞的半数抑制浓度(IC50值);吖啶橙/溴化乙啶(AO/EB)染色观察细胞凋亡;Mito Tracker Red CMXRos染色观察线粒体膜电位(ΔΨm)的改变;Western Blot法检测不同剂量VES对人胃癌SGC-7901细胞Bid、Bax、Bcl-2蛋白表达和细胞色素C(cytochrome C,Cyt C)蛋白表达与定位的影响。结果:VES对SGC-7901细胞的IC50值为101.45μg/ml;VES可引起SGC-7901细胞发生凋亡和线粒体膜电位下降;并引起Cyt C蛋白在细胞内重新定位、Bid蛋白剪切活化、Bax蛋白表达增加和Bcl-2蛋白表达减少。结论:VES可抑制SGC-7901细胞的生长,并通过线粒体途径诱导凋亡,其机制可能是通过剪切活化Bid蛋白、上调Bax/Bcl-2相对水平来实现的。Objective： To study roles of mitochondria and Bcl-2 family proteins in vitamin E succinateinduced apoptosis of human gastric carcinoma SGC-7901 cells. Method： The inhibitory concentration 50%（IC50） of VES in SGC-7901 cell apoptosis was observed by MTT. Fluorescent staining was used to detect apoptosis and the changes of mitochondrial transmembrane potential（△ψm） of the cells. The expressions of Bid, Bax, Bcl-2 and cytochrome C proteins were measured by Western blot after the cells were treated with VES at doses of 5, 10, 20μg/ml respectively. The redistribution of cytochrome C between the mitochondrial and the cytosolic fractions was observed by Western blot after the cells were treated with 20μg/ml VES for 24h. Results： The IC50 of VES in SGC-7901 ceils was 101.45 μg/ml. VES caused apoptosis and the loss of mitochondrial transmembrane potential（△ψm）. Western blot analysis demonstrated that the levels of cytochrome C in four different groups were similar. After the cells were treated with 20μg/ml VES for 24h, cytochrome C was released from mitochondria to cytosol. The expression of Bid in the four groups were similar, but Bid was cleaved into its active form tBid in 10μg/ml and 20 μg/ml group. The expression of Bax in the cells was markedly increased and Bcl-2 decreased, which resulted in the increase of the ratio of Bax/Bcl-2. Conclusion： VES can induce apoptosis of SGC-7901 cells through mitochondrion pathway by activating Bid and up-regulating Bax/Bcl-2.

关 键 词：维生素E琥珀酸酯 胃癌 BID BAX Bol-2 CYT C 

分 类 号：R735.2[医药卫生—肿瘤]