Analysis of Helicobacter pylori and nonsteroidal anti‐inflammatory drug‐induced gastric epithelial injury

Background: Helicobacter pylori and nonsteroidal anti‐inflammatory drugs (NSAIDs) are important factors in gastric mucosal injury. However, the relationship between H. pylori and NSAID‐related gastroduodenal mucosal injury has not been clarified. Aim: To determine the role of H. pylori in NSAID‐induced gastric mucosal injury and to examine the effects of H. pylori , indomethacin and sofalcone on gastric epithelial cells in culture, as a useful model to study gastric mucosal injury. In addition, we studied the effect of sofalcone, a gastric mucosal protection agent, on H. pylori and NSAID‐induced gastric mucosal injury. Methods: Cytotoxic and noncytotoxic strains of H. pylori were used, each with an inoculum of 10 7 cfu/mL. The effect on the growth of RGM–1 cells (a rat gastric epithelial cell line) was studied by MTT assay, and levels of prostaglandin E 2 in culture supernatants were measured by EIA. Results: Both cytotoxic and noncytotoxic strains of H. pylori tended to induce cell injury in RGM‐1 cells at 48 h after inoculation. Indomethacin alone induced gastric epithelial injury in a dose‐dependent manner, but did not augment cell injury induced by H. pylori . In addition, sofalcone (10 −5 mol/L) showed a suppressive effect on indomethacin‐induced gastric epithelial injury. Conclusion: These findings indicate that indomethacin induces gastric mucosal injury regardless of H. pylori infection, and suggests that sofalcone may be a useful drug in the treatment of NSAID‐induced mucosal injury.