Involvement of cyclooxygenase-2 in hyperplastic gastritis induced by Helicobacter pylori infection in C57BL/6 mice

Authors


Dr Furuta, First Department of Medicine, Hamamatsu University School of Medicine, 3600 Handa-cho, Hamamatsu, 431–3192, Japan. E-mail: furuta@hama-med.ac.jp

Abstract

Background and aims:

The hyperplastic changes observed in Helicobacter pylori-associated gastritis have been considered to increase the risk of gastric cancer. The aim of this study was to determine whether cyclooxygenase-2 is involved in the hyperplastic changes in mice infected with H. pylori.

Methods:

Seven-week-old, male C57BL/6 mice (n=40) were inoculated with the Sydney strain of H. pylori. Control mice (n=40) were treated with vehicle only. Half of the infected and control mice were fed an experimental diet containing etodolac (10 mg/kg/day) from 1 week after inoculation until the end of the experiment. The thickness of gastric pits, COX-2 mRNA and protein levels, and prostaglandin E2 (PGE2) levels in the gastric mucosa were determined before and 12, and 24 weeks after inoculation.

Results:

The thickness of gastric pits, COX-2 mRNA and protein levels, and PGE2 levels were significantly increased at 24 weeks after inoculation of H. pylori compared with the control groups. Treatment with etodolac resulted in significant decreases in PGE2 production and in the thickness of gastric pits in the infected groups at 24 weeks after inoculation.

Conclusions:

Our findings suggest that COX-2 is involved in the development of hyperplastic gastritis caused by H. pylori infection via the production of PGE2.

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