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Effects of Aspirin on the Development of Helicobacter pylori ‐Induced Gastric Inflammation and Heterotopic Proliferative Glands in Mongolian Gerbils
Author(s) -
Li Guo Qing,
Xia Harry H. X.,
Chen Min Hu,
Tsukamoto Tetsuya,
Tatematsu Masae,
Gu Qing,
Qiao Liang,
Cho C. H.,
So Wallace H. L.,
Yuen M. F.,
Hu Pin Jin,
Liang Ying Jie,
Lin Han Liang,
Chan Annie O. O.,
Wong Benjamin C. Y.
Publication year - 2008
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.2008.00585.x
Subject(s) - aspirin , helicobacter pylori , gastritis , apoptosis , inflammation , medicine , gastric mucosa , stomach , hyperplasia , gastroenterology , biology , biochemistry
Background: Helicobacter pylori infection is a major cause of gastritis and gastric carcinoma. Aspirin has anti‐inflammatory and antineoplastic activity. The aim of the present study was to determine the effects of aspirin on H. pylori ‐induced gastritis and the development of heterotopic proliferative glands. Methods: H. pylori strain SS1 was inoculated into the stomachs of Mongolian gerbils. Two weeks after inoculation, the animals were fed with the powder diets containing 0 p.p.m. (n = 10), 150 p.p.m. (n = 10), or 500 p.p.m. (n = 10) aspirin. Mongolian gerbils were killed after 36 weeks of infection. Uninfected Mongolian gerbils (n = 10) were used as controls. Histologic changes, epithelial cell proliferation and apoptosis, and prostaglandin E 2 (PGE 2 ) levels of gastric tissue were determined. Results: H. pylori infection induced gastric inflammation. Administration of aspirin did not change H. pylori ‐induced gastritis, but alleviated H. pylori ‐induced hyperplasia and the development of heterotopic proliferative glands. Administration of aspirin accelerated H. pylori ‐associated apoptosis but decreased H. pylori ‐associated cell proliferation. In addition, the increased gastric PGE 2 levels due to H. pylori infection were suppressed by treatment with aspirin, especially at the dose of 500 p.p.m. Conclusions: Aspirin alleviates H. pylori ‐induced hyperplasia and the development of heterotopic proliferative glands. Moreover, aspirin increases H. pylori ‐induced apoptosis. We demonstrated the antineoplastic activities of aspirin in H. pylori ‐related gastric carcinogenesis.