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 10⁷ 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 E₂ 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.