摘要
幽门螺杆菌(H.pylori)感染,特别是CagA^+株感染,与胃癌的发生密切相关,但其分子机制仍不清楚。对H.pylori致胃黏膜癌变的分子机制进行深入研究,结果显示胃黏膜H.pylori感染可增加胃癌的易感性,导致线粒体DNA微卫星不稳(mtMSI)和线粒体DNA核内整合,使线粒体细胞色素氧化酶(COX)Ⅰ、COXⅡ、COXⅢmRNA表达下调,Bid和Bax表达上调。提示H.pylori通过线粒体途径影响细胞凋亡,导致细胞增殖和凋亡的失衡,从分子水平揭示了H.pylori诱导胃癌发生的机制。
Helicobacter pylori （H. priori） infection, especially the CagA^＋ strain, has shown associated with gastric cancer, but its molecular mechanism remains unclear. Therefore the role of H. priori in gastric carcinogenesis is explored, and the results have shown that H. priori infection is associated with an increased risk of susceptibility to gastric cancer, leading to mitochondrial DNA microsatellite instability （mtMSI） and integration of mitochondrial DNA within the nuclei, and affected mitochondrial function by down-regulating the expressions of mitochondrial encoding cytochrome oxidase （COX） Ⅰ, COX Ⅱ and COX Ⅲ mRNA and up-regulating Bid and Bax expressions. H. pylori induces apoptosis through mitochondrial pathway, leading to disturbance of cell proliferation and apoptosis, which further reveal the mechanism of gastric carcinogenesis induced by H. pylori on molecular level.
出处
《胃肠病学》
2007年第10期581-584,共4页
Chinese Journal of Gastroenterology
关键词
胃肿瘤
螺杆菌
幽门
分子作用机制
Stomach Neoplasms
Helicobacterpylori
Molecular Mechanisms of Action
