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

Abstract

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. 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. 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 E2 in culture supernatants were measured by EIA. 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. 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.