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目的 观察幽门螺杆菌 (Hp)感染在正常粘膜演变为胃癌过程中对细胞增殖和凋亡的作用及 Cag A基因对细胞增殖和凋亡的影响 ,进而探讨 Hp增加胃癌发生危险性的机制。 方法 研究对象为 Hp阳性与阴性的慢性浅表性胃炎 (CSG,n=5 6 )、慢性萎缩性胃炎 (CAG,n=2 0 )、慢性萎缩性胃炎伴肠上皮化生 (CAGIM,n=16 )、不典型增生 (DYS,n=18)、胃癌 (GC,n=17)患者及正常对照组 (NS,n=14)。应用 ki- 6 7免疫组化技术评价胃幽门窦上皮细胞增生 ,用切口末端标记法 (TU NEL)检测胃上皮细胞凋亡 ,应用聚合酶链反应 (PCR)技术检测 Hp的 Cag A基因 ,以对 Hp进行基因分型。 结果 Hp阳性患者 (n=75 )的增殖指数 (L I)和凋亡指数 (AI)显著高于 Hp阴性者 (n=5 2 )或正常人 (P<0 .0 5和 P<0 .0 1)。 CSGHp阳性的 L I和 AI明显高于 Hp阴性者 (P<0 .0 1) ,而其余四种胃病 Hp阳性的 L I或 AI与 Hp阴性者比较均无显著性差异。五种胃病无论 Hp阳性与阴性的 L I均较 NS组高 (P<0 .0 1) ,但五种胃病只有 CSG(不论 Hp阳性或阴性 )的 AI较 NS组高 (P<0 .0 1) ,其余四种胃病无论 Hp阳性或阴性的 AI与 NS组比较均差异无显著性 (P>0 .0 5 )。 Cag A+ Hp感染者的 L I明显高于 Cag A- Hp感染者 (P<0 .0 5 ) ,而 AI则明显低于 Cag A- Hp患者
Objective To observe the effect of Helicobacter pylori (Hp) infection on cell proliferation and apoptosis in the process of gastric mucosa evolving into gastric cancer and the effect of Cag A gene on cell proliferation and apoptosis, and to explore the mechanism of Hp increasing the risk of gastric cancer. Methods The subjects were Hp positive and negative chronic superficial gastritis (CSG, n = 5 6), chronic atrophic gastritis (CAG, n = 20), chronic atrophic gastritis with intestinal metaplasia (CAGIM, n = 16), dysplasia (DYS, n = 18), gastric cancer (GC, n = 17) and normal control group (NS, n = 14). The expression of Cag A gene in Hp was detected by polymerase chain reaction (PCR). The expression of Cag A gene in Hp was detected by TUNEL. Hp was genotyped. Results The proliferation index (LI) and apoptosis index (AI) of Hp positive patients (n = 75) were significantly higher than those of Hp negative patients (n = 52) or normal subjects 1). CSGHp positive L I and AI were significantly higher than Hp negative (P <0.01), while the other four stomach Hp positive L I or AI and Hp negative no significant difference. Five gastritis patients had higher Hp positive and negative LI than NS group (P <0.01), but the AI of the five gastritis patients with CSG (positive or negative Hp) was higher than that of NS group (P <0.01) ). There was no significant difference between Hp positive and negative AI in the other four stomach diseases and NS group (P> 0.05). The L I in Cag A + Hp infected patients was significantly higher than that in Cag A-Hp infected patients (P <0.05), while AI was significantly lower in patients with Cag A-Hp