iNOS、p53在幽门螺杆菌相关胃病中的表达

The expression of iNOS,p53 in Helicobacter pylori associated gastric diseases

关键词:  幽门螺杆菌  诱生型一氧化氮合酶  突变型p53蛋白  细胞 凋亡

Key words:  Helicobacter pylori  inducible nitric oxide synthase  p53  apoptosis

摘要:

研究幽门螺杆菌(Hpylori)感染时不同胃粘膜病变中诱生型一氧化氮合酶(iNOS)与p53的表达情况，探讨Hpylori感染与胃癌形成的分子机制。方法：采用免疫组化法检测126例患者胃粘膜iNOS与p 53的表达情况。Hpylori检测采用尿素酶试验法和Warthin—Starry银染法。结果：126例患者中H pylori阳性72例，Hpylori阴性54例。iNOS在炎性细胞的表达率CSG和CAG组明显高于DyS和GC级(P＜0.05)。iNOS在腺上皮细胞的表达率DyS和GC组明显高于CSG和CAG组(P＜0.05)。结论：炎性细胞来源的iNOS起引发凋亡的作用，而腺上皮细胞产生的iNOS有抑制凋亡的作用。H pylori感染激活iNOS通过p53介导凋亡可能是H pylori诱发癌变的机制之一。

Abstract:

To investigate inducible nitric oxide synthase (iNOS)and p53 level at different Helicobacter pylori(Hpylori)associated gastric diseases;to elucilate the biological mechanism of Hpylori infection in gastric carcinogenesis. Methods:The expression and localization of iNOS and p53 were detected in 126 patients respectively by immunohistochemical staining technique.The status of H pylori was detected by warthin-starry silver staining and Urase test methods. Results: The expression of iNOS by inflammatory leucocytes in CSG and CAG group was significantly higher than that in DyS and GC group(P＜0.05). The expression of iNOS by gastric mucosal cells in DyS and GC was significantly higher than that in CSG and CAG (P＜0.05). Conclusions:Our results suggests that iNOS derived from inflammatory leucocytes might induce apoptosis,while iNOS produced by gastricmucosal cells might delay apoptosis. It might be a novel gastric carcinogenesis mechanism that iNOS are involved in the mucosal response to H pylori infection by accumulation of p53 and p53 induce apoptosis.