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Helicobacter pylori-infected animal models are extremely suitable for the investigation of gastric carcinogenesis

机译:幽门螺杆菌感染的动物模型非常适合研究胃癌的发生

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摘要

Although various animal models have been developed to clarify gastric carcinogenesis, apparent mechanism of gastric cancer was not clarified in recent years. Since the recognition of the pathogenicity of Helicobacter pylori (H pylori), several animal models with H pylori infection have been developed to confirm the association between H pylori and gastric cancer. Nonhuman primate and rodent models were suitable for this study. Japanese monkey model revealed atrophic gastritis and p53 mutation after long-term infection of H pylori. Mongolian gerbil model showed the development of gastric carcinoma with H pylori infection alone, as well as with combination of chemical carcinogens, such as N-methyl-N-nitrosourea and N-methyl-N-nitro-N'-nitrosoguanidine. The histopathological changes of these animal models after H pylori inoculation are closely similar to those in human beings with H pylori infection. Eradication therapy attenuated the development of gastric cancer in H pylori-infected Mongolian gerbil. Although several features of animal models differ from those seen in human beings, these experimental models provide a starting point for further studies to clarify the mechanism of gastric carcinogenesis as a result of H pylori infection and assist the planning of eradication therapy to prevent gastric carcinoma.
机译:尽管已经开发出多种动物模型来阐明胃癌的发生,但近年来胃癌的表观机制尚不清楚。自从认识到幽门螺杆菌(H pylori)的致病性以来,已经开发了数种具有幽门螺杆菌感染的动物模型以证实幽门螺杆菌与胃癌之间的关联。非人类的灵长类和啮齿动物模型适用于本研究。日本猴模型显示幽门螺杆菌长期感染后萎缩性胃炎和p53突变。蒙古沙鼠模型显示出胃癌仅由幽门螺杆菌感染以及与化学致癌物(例如N-甲基-N-亚硝基脲和N-甲基-N-硝基-N'-亚硝基胍)的组合发展而成。接种幽门螺杆菌后,这些动物模型的组织病理学变化与感染幽门螺杆菌的人的组织病理学变化非常相似。根除疗法减弱了幽门螺杆菌感染的蒙古沙鼠胃癌的发展。尽管动物模型的某些特征与人类所见的特征不同,但这些实验模型为进一步研究阐明幽门螺杆菌感染导致的胃癌发生机理和协助制定根除疗法以预防胃癌提供了起点。

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