Summary Background: There is compelling evidence for the pivotal role of Helicobacter pylori in the pathogenesis of gastrointestinal ulcer disease. However, despite the bacterium's toxicity, the majority of H. pylori infections are not accompanied by gastric ulcers. This implies the existence of a host mechanism offsetting H. pylori toxicity. Aims: To evaluate gastric fibroblasts' expression of hepatocyte growth factor (HGF), which is known to facilitate gastric ulcer healing, in the presence of H. pylori; to compare the effect on H. pylori‐induced HGF expression of a COX‐2 selective inhibitor with that of nonselective nonsteroidal anti‐inflammatory drugs (NSAIDs). Methods: Human gastric fibroblasts were cultured from human gastric mucosa obtained at surgery. Prostaglandin E2 (PGE2) and HGF were measured by EIA. The expression of COX‐2 mRNA was assessed by the TaqMan quantitative RT‐PCR system. Results: H. pylori increased PGE2 release in gastric fibroblasts. H. pylori induced expression of COX‐2 mRNA, which indicates that PG induction by H. pylori is through COX‐2. Sulindac sulphide, etodolac and NS 398 all inhibited H. pylori‐induced PGE2 release to the same extent. These agents also inhibited H. pylori‐induced HGF release. Conclusion: Gastric fibroblasts produce PG and HGF in response to the presence of H. pylori, which may be considered part of the human body's defensive reaction to H. pylori toxicity. This defensive mechanism is inhibited not only by COX‐2 nonselective NSAIDs but also by a COX‐2 selective inhibitor. These findings indicate the importance of COX‐2 in chronic H. pylori infection.

EPA has a direct protective effect on rat hepatocytes, which is in agreement with the clinical efficacy of EPA in PBC patients.

SUMMARYBackground: Glucocorticoids have been shown to induce peptic ulcers, especially when co-administered with NSAIDs. Hepatocyte growth factor (HGF) plays a role in gastric ulcer repair, facilitating the restitution of gastric mucosal epithelial cells. HGF expression is induced by PGs in gastric fibroblasts. We hypothesized that dexamethasone (DEX) may inhibit PG production and HGF expression, thus inhibiting HGF-induced gastric epithelial restitution. Aim: To investigate the effect of DEX on gastric restitution, using cultured gastric cells, the role of HGF in the restitution inhibited by DEX, and the effect of rebamipide on DEX-inhibited restitution.

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