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作 者:卢世云[1] 潘秀珍[1] 彭孝伟[1] 施作霖[2] 林棱[1] 陈明红[1]
机构地区:[1]福建省立医院消化内科,福建省福州市350001 [2]福建省立医院病理科,福建省福州市350001
出 处:《世界华人消化杂志》2000年第4期386-388,共3页World Chinese Journal of Digestology
摘 要: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。AIM To investigate the effects of different genotype Helicobacter pylori (Hp) infection on the gastric epithelial cell proliferation and apoptosis and further investigate the mechanisms of Hp increasing the risk for the development of gastric cancer.METHODS Endoscopic gastric mucosal biopsies were taken from 19 cases of Hp negative chronic superficial gastritis and 37 Hp positive chronic superficial gastritis. The gastric antral epithelial cell proliferation was evaluated by ki-67 immunohistochemical technique and 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 (Al) of Hp positive patients were significantly higher than that of Hp negative patients (17±4 vs 7.3±3.3 and 11.3 ±3.8 vs 6.6±1.2, P<0.01). The LI and Al in cagA positive or cagA negative patients were significantly higher than Hp negative patients. Patients infected with cagA+ Hp (n=27) had significantly higher LI (18.6±5.8 vs 13.8±4.2, P<0.05) and much lower Al (8.9±3.2 vs 12.2 ±4.6, P<0.01) than that infected with cagA- Hp (n = 10). There was no correlation between LI or Al and the severity of gastritis.CONCLUSION Hp infection induced gastric epithelial hyperproliteration and apoptosis. cagA+ Hp and cagA-Hp had different ability of inducing proliferation and apoptosis.
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