Decreased Helicobacter pylori associated gastric carcinogenesis in mice lacking inducible nitric oxide synthase

Abstract
Background and aims: Overproduction of nitric oxide via inducible nitric oxide synthase (iNOS) is suggested to be a significant pathogenic factor in Helicobacter pylori induced gastritis. The purpose of this study was to examine the role of iNOS in H pylori associated gastric carcinogenesis. Methods: Two types of mice were used in this study: iNOS deficient mice (iNOS−/−) and wild-type littermates. Gastric cancer was generated in mice using a combination treatment comprising N-methyl-N-nitrosourea administration and H pylori infection. Fifty weeks after treatment, tumours in gastric tissues from both types of mice were examined using histopathology, immunohistochemistry, and immunoblotting for iNOS and 3-nitrotyrosine. Results: The overall incidence of gastric cancer at week 50 was significantly lower in iNOS−/− compared with iNOS wild-type mice (pConclusions: These findings suggest that iNOS contributes to H pylori associated gastric carcinogenesis in mice.