幽门螺杆菌感染对胃上皮细胞凋亡影响的实验研究

目的在H.pylori长期感染蒙古沙土鼠腺胃模型基础上,探讨H.pylori感染诱致胃癌发生的可能机制.方法采用H.pylori国际标准菌株NCTCli637灌喂蒙古沙土鼠,建立H.pylori长期感染动物模型:用末端脱氧核苷酸转移酶介导的dUTP切口末端标记法(TUNEL)及原位杂交方法检测H.pyiori感染致胃粘膜上皮细胞凋亡的变化。结果成功建立了H.pylori长期感染蒙古沙土鼠腺胃模型,其胃粘膜的组织学变化显示,H.pylori感染可致正常胃粘膜→慢性胃炎→萎缩→肠化生→异型增生的发展过程。H.pylori感染对胃上皮细胞凋亡的影响:接种H.pylori后25周内能引起胃窦粘膜上皮细胞凋亡增加(P<0.05),H.pylori感染45周时,与25周时相比,胃窦粘膜上皮细胞凋亡指数呈逐渐递减的趋势,65周时甚至明显低于正常值(P<0.05):FAS及FASL原位杂交检测结果显示随着H.pylori感染时间的延长,炎症及病变程度的加重,FAS及FASL mRNA的阳性信号表达有逐渐增加的趋势(R<0.05)。结论 H.pylori走植致胃窦粘膜上皮细胞凋亡的异常,对正常胃窦粘膜向不典型增生进展的过程起重要作用;FAS和FASL在mtLNA水平的异常表达可能是H.pylori定植致胃窦粘膜上皮细胞凋亡异常的重要原因.

Effect of H. pylori infection on gastric cell apoptosis

Objectives To explore induce adenocarcinoma mechanism mechanism that H.pytori infectioncan induce adenocarcinoma on the basis of development of Mongolian gerbil model of longterm infection with H.pylori. Methords Development of Mongolian gerbil model of H.pylori long-term infection by inoculating H.pylori NCTC 11637. Experimental study on the mechanism that H.pylori infection can affect gastric cell apoptosis with TUNEL method and hybridism in sith. Results Mongolian gerbil model of H.plori long-term infection was developed successfully. Hybridism in situ of FAS and FASL showed the expression of FAS and FASL showed the expression of FAS mRNA and FASL mRaNA incresed following time prolongation of H.pylori infection(P<0.05). Conclusion cell apoptosis LI increased during 25 weeks with H.pylori infection; and gastric cell apoptosis LI decreased after 45 veeks(P<0.05).Conclusion H.pylori inoculation can induce abnormality of gastric cell apoptosis, which can affect the erocess progressing from chronic gastritis through glandular atrophy, intestinal metaplasis to atypical hyperplasia. The abonrmal expression of FAS and FASL may be the important cause for abnormality of gastric cell apoptosis.