摘要
目的 :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p5 3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 12 6例患者胃粘膜iNOS与p 5 3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 :12 6例患者中H pylori阳性 72例 ,H pylori阴性 5 4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 0 5 )。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 0 5 )。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p5 3介导凋亡可能是H pylori诱发癌变的机制之一。
Objectives: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 gastric mucosal 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.
出处
《大连医科大学学报》
CAS
2001年第3期169-170,173,共3页
Journal of Dalian Medical University
