幽门螺杆菌诱导胃粘膜上皮细胞凋亡和增殖与p53基因表达  

Apoptosis and proliferation induced by Helicobacter pylori and its assoc iation with p53 protein expression in gastric epithelial cells

作　　者：刘海峰[1] 刘为纹[1] 房殿春[1] 高晋华[1] 王振华[1] 

机构地区：[1]第三军医大学西南医院消化科,重庆市400038

出　　处：《世界华人消化杂志》2001年第11期1265-1268,共4页World Chinese Journal of Digestology

基　　金：军队医药卫生"九五"重点课题资助项目(No.96Z047);重庆市应用基础研究基金

摘　　要：目的研究幽门螺杆菌(Helicobacter pylori,Hp)感染后胃粘膜上皮细胞凋亡和增殖的变化,以及突变型p53基因表达变化与胃粘膜上皮细胞增殖和凋亡变化的关系。方法采用脱氧核糖核酸末端转移酶介导的缺口末端标记(TUNEL)技术及免疫组织化学染色对Hp阳性患者Hp根除前后及Hp阴性者胃粘膜上皮细胞凋亡和增殖情况进行原位观察和比较,并对突变型p53基因的表达状况进行检测。结果 Hp阳性患者胃粘膜上皮细胞凋亡指数及PCNA指数(12.7％,14.1％)均显著高于Hp阴性患者(3.0％,8.3％,t=7.241,6.368,P<0.01),Hp根除后胃粘膜上皮细胞PCNA指数和凋亡指数(14.2％,12.7％)均显著下降(9.1％,3.6％,t=5.642,7.410,P<0.01),而Hp未根除者上述指标则无显著性变化。Hp阳性组p53阳性率(39.1％)显著高于Hp阴性组(15.4％,x^2=4.414,P<0.05).Hp阳性组p53阳性者PCNA指数(18.7％)显著高于p53阴性者(11.5％,t=4.185,P<0.01),而p53阳性者细胞凋亡指数(8.4％)显著低于p53阴性者(12.6％,t=3.120,P<0.01)。结论 Hp感染可引起胃粘膜上皮细胞凋亡及增殖的变化,使胃粘膜的不稳定性增加,从而增加患胃癌的危险性,突变型p53基因异常表达可能参与了此过程的调控。AIM To study the relationship between gastric epithelial apoptosis and proliferation induced by Helicobacter pylori and p53 protein expression in H. pylori.related gastritis, analyze the mechanisms of H. pylori infection induced gastric epithelial cell apoptosis as well as proliferation, and explore the role of H. pylori in the development of gastric diseases. METHODS Endoscopic mucosal biopsies were taken in 72 cases of chronic gastritis. Using terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) technique and immunohistochemical staining, we observed the apoptotic cells and proliferative cells in situ in H. pylori negative gastric mucosa, H. pylori positive gastric mucosa before and after H. pylori eradication, and compared the number of apoptotic cells and proliferative cells with the p53 gene expression in each case. RESULTS The apoptotic index and PCNA index of gastric epithelial in the patients infected with H. pylori (12.7% and 14.1%) were significantly higher than those of H. pylori negative gastric epithelial (3.0% and 8.3%, t=7. 241,6.368, P<O.O1). After eradication of H. pylori with triple therapy, the PCNA index and apoptotic index fell from 14.2% and 12.7% to 9.1% and 3.6%(t=5.642,7. 410, P<0.01). In the persisting H. pylori infected patients, the apoptotic index and PCNA index were not statistically decreased. The positive rates of p53 protein of gastric epithelial in the patients infected with H. pylori (39.1%) was significantly higher than that of H. pylori negative gastric epithelial(15.4%(?)=4.414, P<0.05). In the patients infected with H. pylori, the PCNA index in p53 positive group(18.7%) was significantly higher than that in p53 negative group(11.5%, t=4.185, P<0.01) but the apoptotic index in p53 positive group(8.4%) was significantly lower than that in p53 negative group(12. 6%,t=3.120, P<0.01). CONCLUSIONS H. pylori infection did induce gastric epithelial apoptosis and proliferation. H. pylori could increase the expression of mutant p53 protein, this may be one of the m

关 键 词：幽门螺杆菌 增殖 胃粘膜上皮细胞凋亡 

分 类 号：R573[医药卫生—消化系统]