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目的 观察幽门螺杆菌 (Hp)及其 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 119例慢性胃炎患者 ,其中 Hp阳性 6 8例 ,Hp阴性 5 1例。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 (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 Cag A基因。结果 Hp阳性患者的增殖指数 (L I)和凋亡指数 (AI)显著高于 Hp阴性者 (P<0 .0 5 )。Cag A+或 Cag A-Hp患者的 L I和 AI均显著高于 Hp-患者 ,Cag A+ Hp患者 (n=5 3)的 L I明显高于 Cag A- Hp患者 (n=15 ) (P<0 .0 5 ) ,而 AI则明显低于 Cag A- Hp患者 (P<0 .0 1)。L I和 AI与胃粘膜炎症程度无明显关系。结论 Hp感染诱导胃粘膜上皮细胞过度增殖和凋亡 ,Cag A+ Hp与 Cag A- Hp促增殖和凋亡作用的能力明显不同 ,Hp感染通过引起增殖和凋亡比例的失调 ,最终促进肿瘤发生。
Objective To observe the effects of Helicobacter pylori (Hp) and 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 119 chronic gastritis patients, of which Hp positive was 68 and Hp negative was 51. The proliferation of gastric pyloric sinusoidal epithelial cells was evaluated by immunohistochemical technique. The apoptosis of gastric epithelial cells was detected by TUNEL. The Cag A gene of Hp was detected by polymerase chain reaction (PCR). Results The proliferation index (L I) and apoptosis index (AI) of Hp positive patients were significantly higher than those of Hp negative patients (P <0.05). LI and AI in patients with Cag A + or Cag A-Hp were significantly higher than those in Hp-patients (P <0.05), and patients with Cag A + Hp (n = 5 3) had significantly higher LI than patients with Cag A-Hp. 0 5), whereas AI was significantly lower in Cag A-Hp patients (P <0.01). L I and AI had no significant relationship with the degree of gastric mucosal inflammation. Conclusion Hp infection induces overgrowth and apoptosis of gastric mucosal epithelial cells. The ability of Cag A + Hp and Cag A-Hp to promote proliferation and apoptosis is obviously different. Hp infection can promote the tumorigenesis by inducing the imbalance of proliferation and apoptosis ratio.