幽门螺杆菌致肝脏病变的2年动物实验观察  

A two-year animal experimental study on the pathological effects of Helicobacterpylori on liver tissues

作　　者：田雪飞[1] 范学工[1] 黄勋[1] 付春燕[2] 代洪[1] 黄燕[1] 

机构地区：[1]中南大学湘雅医院传染科,长沙410008 [2]中南大学湘雅医院病理科,长沙410008

出　　处：《中华肝脏病杂志》2008年第2期129-133,共5页Chinese Journal of Hepatology

基　　金：国家自然科学基金（30271171）

摘　　要：目的探讨幽门螺杆菌（H．pylori）经口接种长期感染后，是否可到达肝脏并作为独立的致病因素导致小鼠肝脏病变，甚至肝癌的发生。方法H．pylori悉尼株（SSI）经口接种C57BL／6小鼠，24个月时处死。检测小鼠胃、肝组织内细菌定植情况与病理改变；提取肝组织内细菌DNA，巢式PCR扩增小鼠肝组织H．pylori 16S rRNA基因，PCR产物测序，并与胃黏膜分离的H．pylori,接种H．pylori SS1的16S rRNA PCR产物测序结果进行同源性比较。结果接种组12只小鼠在胃黏膜检测到H．pylori，11只出现胃组织病理改变，其中1只发生胃淋巴瘤。接种组7只在肝脏检测到H．pylori，6只出现肝脏病理变化，其中1只轻微炎症；3只炎症伴纤维化病变；2只炎症伴纤维化及异型性增生。接种组肝脏H．pylon染色阳性且出现肝脏病理改变小鼠，胃H．pylon染色均呈阳性。接种组肝脏H．pylori染色阴性小鼠和（或）胃H．pylori染色阴性小鼠，以及正常对照组小鼠均未发现肝脏病理改变。肝组织中扩增的H．pylori 16S rRNAPCR产物测序结果经序列分析后显示：与胃黏膜分离培养细菌、接种细菌同源性为100％。结论经口接种H．pylori 2年长期感染后，除导致小鼠胃组织病变外，部分小鼠胃组织感染细菌可到达肝脏，引起肝脏炎症，甚至肝硬化、癌前病变的发生。Objective To observe whether H. pylori administered orally in mice could arrive in their livers after a long-term infection, leading to active inflammation and even causing HCC as an independent etiological factor. Methods Twenty C57BL/6 mice were orally administered H. pylori SS 1 and kept for 24 months （experimental group） along with 13 mice which served as blank controls （control group）. H. pylori colonization and pathologic consequences were studied in the livers and gastric tissues of the mice. The bacterial DNA extracted from liver tissues was examined by nested PCR for H. pylori 16S rRNA genes. 16S rRNA PCR amplicons were sequenced and compared with sequencing results of 16S rRNA PCR amplicons of the bacteria cultured from gastric mucosa and compared with that of the inoculated H. pylori SS 1. Results Of the 20 mice in the experimental group, H. pylori was found in the gastric mucosa of 12, and in 11 of them pathological gastric lesions were found, including one with gastric lymphoma. H. pylori were found in the livers of 7 mice. Liver lesions, one with mild inflammation, 3 with inflammation and fibrosis, 2 with inflammation, fibrosis and hepatocytehyperplasia with atypia were found in 6 of them. No liver lesions were found in the mice of the control group. In the mice of the experimental group no liver lesions were found in those mice with no H. pylori in their gastric mucosae. Sequencing results of 16S rRNA PCR products of the liver showed 100% homogeneity with the cultured H. pylori from gastric mucosa and the administered H. pylori SS 1. Conclusion Two years after oral administration of H. pylori to C57BL/6 mice, gastric mucosal lesions and liver lesions, including inflammation, cirrhosis and hepatocyte hyperplasia with atypia were found in those animals.

关 键 词：螺杆菌 幽门 肝疾病 小鼠 

分 类 号：R575[医药卫生—消化系统] R573.1[医药卫生—内科学]