诱导型一氧化氮合酶、一氧化氮在Hp(+)胃炎中的表达及与细胞凋亡的关系

Increased expression of nitric oxide and inducible nitric oxide synthasein Helicobacter pylori gastritis

目的探讨幽门螺杆菌(Hp)感染时胃黏膜组织NO含量、iNOS表达,并研究它们与细胞凋亡的关系。方法测定10例正常对照,15例Hp阴性慢性胃炎,32例Hp阳性慢性胃炎胃黏膜组织NO含量及iNOS、Bax的表达。结果Hp阳性慢性胃炎组iNOS,Bax的表达、NO含量均明显高于Hp阴性慢性胃炎组及正常对照组;Hp阳性慢性胃炎组iNOS表达、NO含量与胃炎积分数呈正相关,NO含量与iNOS表达之间,iNOS表达与Bax 表达之间亦存在正相关关系。结论Hp感染时胃黏膜NO含量的增加主要来源于iNOS;iNOS、NO参与了Hp所致的胃黏膜细胞凋亡的调控机制,而此作用很可能是通过Bax蛋白或其它细胞凋亡相关基因的参与来实现的。

Objective To investigate the significance of expression of nitric oxide (NO) and inducilie nitric oxide synthase (iNOS) in gastic mucosa of patients with Helicobacter pylori (Hp) infection and the relationship between H. pylori infection, expression of iNOS and the expression of Bax. Methods Using immunohistochemical staining and nitric acid reductase method, we examined the expression of NO and iNOS. Bax in 10 Hp negative normal controls, 15 Hp negative and 32 Hp positive patients with chronic gastritis. Results The expression of NO and iNOS protein in Hp positive chronic gastritis are much higher than that of Hp negative chronic gastritis and normal controls.There is positive correlation between the expression of NO, iNOS and inflammation scores. There is also significance association between the expression of NO and iNOS. iNOS scoring was also statistically significantly correlated with the expression of Bax. Conclusion NO is mainly derived from iNOS in gastric mucosa with Hp infection; iNOS, NO may be involved in the pathogenetic mechanisms of Hp asscociated gastric diseases. iNOS, NO take part in the molecular mechanism in apop-tosis of gastric epithelial cells,this may be executed by Bax protein or other cell apoptosis associated genes.