Abstract

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. 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. 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. 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.

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