Objective By detecting the expression of Helicobacter pylori (Hp), cytotoxic-associated gene A (CagA), P53 and iNOS in chronic superficial gastritis (CSG) , chronic atrophic gastritis (CAG) , intestinal metaplasia (IM) , Dysplasia (DYS) and gastric cancer (GC), we explored the correlation between the expression of Hp, CagA, P53, iNOS and GC, as well as the possible mechanism. Methods The expression of Hp was examined by rapid urease test, gram staining of tissue sections and serum HpCagA antibodies. The expression of CagA gene of Hp was tested by polymerase chain reaction (PCR). The expression of mutant P53 and iNOS proteins was detected by immunohistochemical staining. Results The positive rates of Hp were 46. 7%, 67.2%, 70.0%, 75.3% and 53.8% in CSG, CA, IM, DYS and GC respectively, while the positive rates of CagAgene were 34. 3%, 59. 0%, 65. 7%, 69.1% and 76.8% in the corresponding tissues. The infection rates of Hp in GC groups showed significant differences compared with those in DYS groups (P<0. 05) , and the infection rates of Hp in CAG, IM and DYS groups were significantly different compared with those in CSG groups (P<0. 05). The infection rates in CagA-positive cases of IM,DYS and GC groups were higher than those in CSG groups (P<0. 01-P<0. 05) , and higher in GC groups than in CAG groups (P<0. 05). In the evolution of gastric mucosa from CSG to GC, the expression rates of mutant p53 and iNOS in CagA-positive cases were gradually increasing. Beyond CSG, the expression rates of mutant p53 in CagA-positive cases were significantly higher than those in CagA-nega-tive cases (P<0. 005-P<0. 05). In all five groups, the expression rates of iNOS in CagA-positive cases were consistently higher than those in CagA-negative cases (P<0. 005-P<0. 05). Conclusion Hp and especially CagA are related to the genesis OF of GC and contribute to its development through abnormal expression of iNOS and P53 gene mutation. However, P53 gene mutation is a relatively late event in the development of GC.%目的 通过检测慢性浅表性胃炎(CSG)、慢性萎缩性胃炎(CAG)、肠上皮化生(IM)、不典型增生(DYS)、胃癌(GC)组织幽门螺杆菌(Hp)和细胞毒素相关蛋白A(CagA)基因、P53、一氧化氮合成酶(iNOS)的表达,探讨Hp、CagA基因、P53、iNOS与胃癌相关性及其参与胃癌形成的可能机制.方法 应用快速尿素酶试验和组织切片革兰氏染色和血清HpCagA抗体检测Hp表达,用PCR检测HpCagA基因表达,用免疫组化SP法检测上述组织的突变P53蛋白、iNOS 表达.结果 CSG、CAG、IM、DYS、GC组织中Hp检出率分别为46.7%、67.2%、70.0%、75.3%和53.8%,相应组织中HpCagA检出率分别为34.3%、59.0%、65.7%、69.1%和76.8%,GC组Hp感染率与DYS组相比差异显著(P＜0.05),而CAG、IM、DYS组与CSG组Hp感染率相比差异显著(P＜0.05).IM、DYS、GC组CagA+株感染率则高于CSG组(P＜0.01-P＜0.05),GC组CagA+株感染率则高于CAG组(P＜0.05).从CSG到GC胃粘膜演变中,CagA基因阳性组中的突变P53、iNOS表达逐渐升高;除CSG外,CAG、IM、DYS、GC组CagA基因阳性组突变P53表达明显高于CagA基因阴性组突变P53表达(P＜0.005-P＜0.05);CSG、CAG、IM、DYS、GC组CagA基因阳性组iNOS表达均高于CagA基因阴性组iNOS表达(P＜0.005-P＜0.05).结论 Hp特别是CagA基因与胃癌形成有关,Hp、CagA引起iNOS表达增高,P53基因突变,在形成胃癌中发挥作用,但P53基因突变在胃癌形成中属于较晚期事件.
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