幽门螺杆菌感染对胃上皮细胞增殖影响的实验研究

目的在幽门螺杆菌(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NCTC11637灌喂蒙古沙土鼠,建立H.pylori长期感染动物模型;用免疫组化及原位杂交方法检测H.pylori感染致胃上皮细胞增殖的改变.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感染对胃上皮细胞增殖的影响:H.pylori感染能引起胃窦上皮细胞增殖增加(P<0.05);随着H.pylori感染时间的增加,EGF mRNA及EGFR mRNA的阳性信号表达呈逐渐增加的趋势(P<0.05) H.pylori定植致胃窦上皮细胞增殖的异常,对正常胃窦粘膜向不典型增生进展的过程起重要作用:EGF及EGFR在mRNA水平的异常表达可能是H.pylori定植致胃窦上皮细胞增殖异常的重要原因。

Effect of H. pylori infection on gastric cell proliferation

Objective To explore the mechanism that H. pylori infection can induce adenocarcinoma on the basis of development of Mongolian gerbil model with H. pylori long-term infection. Methods Development of Mongolian gerbil model with H. pylori long-term infection by inoculating H. pylori NCTC 11637. H.pylori infection can affect gastric cell proliferation with the immunohistochemistry straining and hybridization in situ. Results Mongolian gerbil model with H.pylori long-term infection was developed successfully. Immunohistochemistry straining of BrdU and PCNA showed H. pylori infection induced increasion of gastric cell proliferation (P<0.05). Hybridization in situ of EGF and EGFR showed the expression of EGF mRNA and EGFR mRNA increased following time prolongation of H. pylori infection (P<0.05). Conclusion H.pylori inoculation can induce abnormality of gastric cell proliferation, which can affect the process progressing from chronic gastritis through glandular atrophy, intestinal metaplasis to atypical hyperplasia. The abnormal expression of EGF and EGFR may be the important cause for abnormality of gastric cell proliferation.