Effects of selective cyclooxygenase-2 inhibitor and non-selective NSAIDs on Helicobacter pylori-induced gastritis in Mongolian gerbils

Background. It is still a point of controversy whether Helicobacter pylori-infected patients are more likely to develop mucosal damage while taking NSADIs. Selective cyclooxygenase (COX-2) inhibitors may be associated with less severe gastric mucosal damage than conventional NSAIDs, but this association is undefined in H. pylori-induced gastritis. The aim of this study was to evaluate the effects of selective COX2 and nonselective NSAIDs on H. pylori-induced gastritis. Methods. After intragastric administration of indomethacin, NS-398 or vehicle alone, once daily for 5 days in H. pylori-infected and uninfected Mongolian gerbils, we evaluated gastric mucosal damage, inflammatory cell infiltration and prostaglandin E-2 (PGE(2)) concentration. We investigated whether H. pylori infection induced the COX-2 expression. Results. In H. pylori-uninfected groups, the indomethacin-treated group showed the highest mucosal damage score and the lowest PGE(2) concentration. There was no difference in mucosal damage scores and PGE(2) concentration between NS-398 and vehicle-alone treated group. In H, pylori-infected groups, there was no difference in mucosal damage scores, irrespective of the type of drugs administered. The indomethacin-treated group showed the lowest PGE(2) concentration, similar to that of the NS-398 and vehicle-alone treated groups, both without H. pylori infection. Gastric neutrophil and monocyte infiltration scores were higher in H. pylori-infected groups than in uninfected groups. However, there was no difference in these scores according to the type of drugs administered, within H. pylori-infected or uninfectcd groups. COX-2 protein expression was observed in H. pylori-infectcd Mongolian gerbils but not in uninfectcd ones. Conclusions. Our animal study showed that H. pylon infection induced COX-2 expression and increased prostaglandin concentration. Administration of NSAIDs decreased the prostaglandin concentration, but did not increase mucosal damage in H. pylori-induced gastritis. Selective COX-2 inhibitors, instead of conventional NSIADs, had no beneficial effect on preventing mucosal damage in H. pylori-induced gastritis.