幽门螺杆菌相关性胃病的细胞增殖和凋亡

目的 观察幽门螺杆菌（Hp)及其CagA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 研究对象为慢性浅表性胃炎（CSG）、慢性萎缩性胃炎（CAG）、慢性萎缩性胃炎伴肠上皮化生（CAGIM）、不典型增生（DYS）、胃癌（GC）患者127例及正常对照组（NS）14例。应用ki-67免疫组化技术评价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阴性者或正常对照（P＜0．05和P＜0．01）。CSGHp阳性的LI和AI明显高于Hp阴性者（P＜0．01），而其余四种胃病Hp阳性患者（P＜0．05）。Hp阳性或阴性CSG、NS组的AI与LI呈正相关，GC患者的AI与LI呈负相关。LI和AI与胃粘膜炎症程度无明显关系。结论 Hp诱导胃粘膜上皮细胞过度增殖和凋亡主要发生在Hp感染的早期，CagA^ Hp与CagA^－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。

The cell proliferation and apoptosis in Helicobacter pylori associated diseases of the stomach

Aim To investigate the effects of Helicobacter pylori(Hp) infection and CagA gene on the gastric epithelial cell proliferation and apoptosis, and investigate the mechanisms of Hp increasing the risk of development of gastric cancer.Methods Endoscopic gastric mucosal biopsies were taken from 127 patients(chronic superficial gastritis,CSG; chronic atrophic gastritis,CAG; chronic atrophic gastritis with intestinal metaplasia,CAGIM; dysplasia,DYS; gastric cancer,GC) and 14 normal subjects(NS).The gastric antral epithelial cell proliferation was evaluated by ki-67 immunohistochemical technique, apoptosis cells in the gastric mucosa were quantitated after terminal deoxynucleotidyl transferase mediated dUTP nick end-labelling and Hp CagA gene was detected by polymerase chain reaction(PCR).Results Ki-67 labelling index(LI) and apoptosis index(AI) of Hp positive patients were significantly higher than that of Hp negative patients or normal controls( P <0.05 and P<0.01) .The LI and AI in Hp positive CSG patients were significantly higher than that in Hp negative CSG patients ( P<0.01); there was no significant difference between the patients with Hp infection and without Hp infection of the other four groups.Patients infected with CagA Hp had significantly higher LI and much lower AI than that infected with CagA - Hp( P<0.05 ).The AI and LI had a positive correlation in Hp positive or negative CSG group and NS group, and a negative correlation in GC group.There was no correlation between LI or AI and the severity of gastritis.Conclusions Hp induced gastric epithelial proliferation and apoptosis predominantly in the early stage of Hp infection.CagA Hp and CagA - Hp had different ability of inducing proliferation and apoptosis.Hp infection might lead to the imbalance of the AI/LI ratio and ultimately promote the development of gastric cancer.