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Abstract
Background: Nitric oxide (NO) plays an important role in gastrointestinal mucosal protection. We have previously shown that Helicobacter pylori infection is associated with a lower concentration of NO in the human stomach. The aim of this study is to explore the pathogenesis of this finding using an animal model. Methods: Mongolian gerbils were divided into four groups: H. pylori-negative and -positive, each with and without the intraperitoneal addition of superoxide dismutase (SOD). Intraluminal NO and serum nitrate were measured by using a chemiluminescence system. Inducible nitric oxide synthase (iNOS) levels in gastric mucosa were measured by using the NOSdetect Assay Kit. Results: iNOS levels in H. pylori-positive gerbils were significantly greater than in those without infection. Intraluminal NO levels in H. pylori-positive gerbils were significantly lower than those in H. pylori-negative ones and increased after SOD administration. Serum nitrate levels in H. pylori-positive gerbils were significantly greater than those in H. pylori negative ones and decreased after SOD administration. Conclusions: The low level of NO in the gastric lumen in H. pylori infection is likely a result of superoxide production related to H. pylori-induced inflammation.