CagA^+幽门螺杆菌与胃黏膜上皮细胞凋亡的分子研究  

The Molecular Mechanism of Apoptosis in Gastric Epithelial Cell Induced by CagA^+ Helicobacter Pylori

作　　者：周海波[1] 颜云[2] 颜世军 朱菊人[1] 

机构地区：[1]山东省立医院消化内科,济南250022 [2]山东省潍坊市人民医院,潍坊261041 [3]山东省临朐县朐山医院,临朐267000

出　　处：《中国临床医学》2002年第6期614-616,共3页Chinese Journal of Clinical Medicine

摘　　要：目的:观察CagA^+Hp对胃黏膜上皮细胞凋亡的影响,进而探讨CagA^+Hp增加胃癌发生危险性的机制。方法:以TUNEL染色法研究30例CagA^+Hp阳性患者Hp根除前后胃黏膜上皮细胞凋亡的情况;通过免疫组织化学法和RT—PCR检测凋亡相关基因bcl—2和bax的表达。结果:CagA^+Hp阳性患者胃黏膜上皮细胞凋亡指数为13.42％,Hp根除后,胃黏膜上皮细胞凋亡指数降为4.8％,较治疗前明显减少(P<0.01),而CagA^+Hp仍为阳性患者胃黏膜上皮细胞凋亡指数无明显减少(P>0.05);bcl—2蛋白表达阳性的CagA^+Hp阳性患者Hp根除后,胃黏膜上皮细胞bcl—2蛋白表达阳性明显增多(P<0.01),且胃黏膜上皮细胞bcl—2的mRNA表达明显增强(P<0.01),而CagA^+Hp仍为阳性患者冒黏膜上皮细胞bcl—2蛋白表达和mRNA表达无明显增强(P>0.05);bax蛋白表达阳性的CagA^+Hp阳性患者Hp根除后,胃黏膜上皮细胞bax蛋白表达阳性明显减少(P<0.01),且胃黏膜上皮细胞bax的mRNA表达明显减少(P<0.01);而CagA^+Hp仍为阳性患者胃黏膜上皮细胞bax蛋白表达和mRNA表达无明显减少(P>0.05)。结论:诱导胃黏膜上皮细胞凋亡是CagA^+Hp参与胃癌发生的机制之一,CagA^+Hp通过下调bcl—2的表达、促进bax的表达诱导胃黏膜上皮细胞凋亡。Objective: To investigate apoptosis in gastric epithelial cell induced by CagA+ Helicobacter pylori, and discuss the relation between cell apoptosis and expression of bcl-2 and bax. Methods :TUNEL staining method were used to detect the apoptosis status of gastric epithelial cell induced by CagA+ Helicobacter pylori. Immunohistochemical staining and RT-PCR were used to detect the expression of apoptosis - regulated gene bcl-2 and bax. Results: After eradication of CagA+ Hp with triple therapy , the apoptotic index fell from 13.42% to 4. 8% (P<0.01) , but in the persisting CagA+ Hp infected patients, the apoptotic index was not statistically decreased (F,0.05): the positive cell of bcl-2 protein and mRNA of bcl -2 was statistically increased (P<0.01), but in the persisting CagA+ Hp infected patients, the positive cell of bcl -2 protein and mRNA of bcl-2 was not statistically increased (P >0. 05): the positive cell of bax protein and mRNA of bax was statistically decreased (P<0.01), but in the persisting CagA+ Hp infected patients, the positive cell of bax protein and mRNA of bax was not statistically decreased (P>0.05). Conclusion: CagA+ Helicobacter pylori induces the apoptosis of gastric epithelial cell. This apoptosis may be mediated by decreasce expression of apoptosis - regulated gene bcl - 2 and increased expression of apoptosis - regulated gene bax.

关 键 词：幽门螺杆菌 CAGA基因 胃黏膜 细胞凋亡 胃癌 发病机制 

分 类 号：R735.2[医药卫生—肿瘤]