线粒体损伤在幽门螺杆菌诱导胃癌细胞凋亡中的作用  

The role of mitochondrial damages in Helecobacter pylori-induced apoptosis of gastric cancer cells

作　　者：兰春慧[1] 房殿春[1] 樊丽琳[1] 贺志高[1] 陈东风[1] 刘重阳[1] 史洪涛[1] 

机构地区：[1]第三军医大学附属西南医院全军消化专科中心,重庆400038

出　　处：《中华内科杂志》2005年第10期748-750,共3页Chinese Journal of Internal Medicine

基　　金：国家自然科学基金(30070043);全军"十五"重点基金资助项目(01Z075)

摘　　要：目的研究线粒体途径在幽门螺杆菌(Hp)诱导胃癌细胞凋亡过程中的作用。方法采用Westernblotting检测细胞内线粒体DNA细胞色素氧化酶(COX)Ⅰ蛋白表达的含量;流式细胞术测定细胞凋亡和线粒体膜电位变化。结果Hp培养滤液呈剂量和时间依赖性地直接诱导SGC-7901细胞凋亡,随着其浓度的增加,细胞的凋亡率呈上升的趋势。Hp培养滤液处理SGC-7901细胞4h后,线粒体膜电位开始降低,8h后下降更明显,12h已基本降至最低,24h后无明显变化。Hp培养滤液作用胃癌细胞后,线粒体DNACOXⅠ蛋白表达明显低于对照组(632·8±40·6vs895·1±44·2,P<0·05)。结论线粒体途径可能在Hp诱导SGC-7901胃癌细胞凋亡过程中起重要作用。Objective To explain the role of mitochondrial pathway in the apoptosis of SGC-7901 cell line induced by concentrated Helecobacter pylori culture supernatant （CHCS）. Methods Cytochrome oxidase（COX） I expression was detected by Western blotting. Cell apoptosis and mitochondrial membrane potential were measured by flow cytometry. Results CHCS could induce the apoptosis of SGC-7901 in a dose- and time-dependent manner. Apoptotic rates gradually enhanced followed by the concentrations increasing. The mitochondrial membrane potential （MMP） began to descend after treating CHCS for 4 h, and MMP descended most distinctly in 8 h. It descended the lowest point in 12 h, and it had no special changes in 24 h, The expression of COX I was notably lower than that of control group after CHCS treating （632. 8±40. 6 vs 895.1 ± 44, 2, P 〈 0. 05 ）. Conclusion Mitochondrial pathway may play an important role in the apoptosis of SGC-7901 cells induced by CHCS.

关 键 词：螺杆菌 幽门 脱噬作用 氧化还原酶类 

分 类 号：R735.2[医药卫生—肿瘤]