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目的 观察不同基因型Hp感染对胃上皮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19例Hp阴性的慢性浅表性胃炎和37例Hp阳性的慢性浅表性胃炎患者,应用ki-67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(TUNEL)检测胃上皮细胞凋亡,应用聚合酶链反应(PCR)技术检测Hp的cagA基因。 结果 Hp阳性患者的增殖指数(LI)和凋亡指数(AI)显著高于Hp阴性者(17±4对7.3±3.3和11.3±3.8对6.6±1.2,P<0.01),cagA~+或cagA~-Hp患者的LI和AI均显著高于Hp~-患者,cagA~+Hp患者(n=27)的LI明显高于cagA~-Hp患者(n=10)(18.6±5.8对13.8±4.2,P<0.05),而AI则明显低于cagA~-Hp患者(8.9±3.2对12.2±4.6,P<0.01),LI和AI与胃粘膜炎症程度无明显关系。 结论 Hp感染诱导胃上皮细胞过度增殖和凋亡,cagA~+Hp与cagA~-Hp促增殖和凋亡作用的能力明显不同。
Objective To observe the effects of different genotypes of Hp infection on the proliferation and apoptosis of gastric epithelial cells, and to explore the mechanism of Hp increasing the risk of gastric cancer. Methods Nineteen Hp-negative chronic superficial gastritis and 37 Hp-positive chronic superficial gastritis were studied. The ki-67 immunohistochemical method was used to evaluate the proliferation of gastric pyloric sinusoidal epithelial cells. TUNEL ) To detect gastric epithelial cell apoptosis, Hp cagA gene was detected by polymerase chain reaction (PCR). Results The proliferation index (LI) and apoptosis index (AI) in Hp positive patients were significantly higher than those in Hp negative patients (17 ± 4 vs. 7.3 ± 3.3 and 11.3 ± 3.8 vs 6.6 ± 1.2, P <0.01), cagA ~ + or cagA The LI and AI in ~ -Hp patients were significantly higher than those in Hp ~ - patients. The LI in cagA ~ + Hp patients (n = 27) was significantly higher than that in cagA ~ -Hp patients (n = 10) (18.6 ± 5.8 vs 13.8 ± 4.2 , P <0.05), while AI was significantly lower in patients with cagA ~ -Hp (8.9 ± 3.2 vs 12.2 ± 4.6, P <0.01). There was no significant correlation between LI and AI and gastric mucosal inflammation. Conclusions Hp infection induced excessive proliferation and apoptosis of gastric epithelial cells. The ability of cagA ~ + Hp and cagA ~ -Hp to promote proliferation and apoptosis was significantly different.