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目的研究幽门螺杆菌(H·pylori,Hp)感染与环氧化酶-2(COX-2)、诱导型一氧化氮合酶(iNOS)表达之间的关系,以探讨Hp的致病及可能致癌机制。方法2005年6月至2006年5月,南昌大学第一附属医院消化内科采用免疫组化法检测294例胃黏膜标本中COX-2、iNOS的表达。结果(1)各研究组和对照组间炎症细胞和腺细胞中COX-2阳性积分差异均有显著性(P<0·01),其中以肠上皮化生与异性增生(IM+DYS)组最高;且浅表性胃炎(CSG)和IM+DYS组Hp阳性者炎症细胞中COX-2表达明显高于Hp阴性(P<0·05)。(2)各研究组和对照组间炎症细胞中iNOS的阳性积分差异有显著性(P<0·05),其中以CSG组最高,IM+DYS组次之;在CSG和IM+DYS组Hp阳性者炎症细胞中iNOS表达明显高于Hp阴性(P<0·05)。(3)中重度CSG炎症细胞中iNOS表达高于轻度CSG(P<0·05)。(4)各研究组胃黏膜中COX-2和iNOS的表达呈显著正相关(P<0·01)。结论(1)Hp感染可能通过诱导COX-2、iNOS的过度表达参与Hp的致病过程,并且Hp可能通过上调COX-2的过度表达参与胃癌发生的早期进程。(2)COX-2、iNOS的表达在Hp的致病过程中相互作用,相互影响。
Objective To study the relationship between H. pylori (Hp) infection and the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in order to explore the possible pathogenesis of Hp Carcinogenic mechanism. Methods From June 2005 to May 2006, immunohistochemistry was used to detect the expression of COX-2 and iNOS in 294 gastric mucosa specimens from the First Affiliated Hospital of Nanchang University. Results (1) There were significant differences in COX-2 positive scores between inflammatory cells and glandular cells in all study groups and control groups (P <0.01), with the highest in intestinal metaplasia and dysplasia group (IM + DYS) , And the expression of COX-2 in Hp-positive inflammatory cells of superficial gastritis (CSG) and IM + DYS group was significantly higher than that of Hp negative (P <0.05). (2) The positive integral of iNOS in inflammatory cells in each study group was significantly different from that in control group (P <0.05), which was highest in CSG group, followed by IM + DYS group, and in Hyp, CSG group and IM + DYS group The positive expression of iNOS in inflammatory cells was significantly higher than that in Hp (P <0.05). (3) The expression of iNOS in moderate-severe CSG inflammatory cells was higher than mild CSG (P <0.05). (4) There was a significant positive correlation between COX-2 and iNOS expression in gastric mucosa (P <0.01) in all study groups. Conclusions (1) Hp infection may be involved in the pathogenesis of Hp by inducing overexpression of COX-2 and iNOS, and Hp may be involved in the early progression of gastric cancer by up-regulating COX-2 overexpression. (2) The expression of COX-2 and iNOS interacted and interacted with each other in the pathogenicity of Hp.