Inhibition of lipid peroxidation, NF-κB activation and IL-8 production by rebamipide in Helicobacter pylori-stimulated gastric epithelial cells

The present study aimed to investigate whether rebamipide, a novel antiulcer agent that has an oxygen radical scavenging activity, would inhibit lipid peroxidation, NF-kappa B activation, and IL-8 production by H. pylori. Human gastric epithelial cells (AGS and KATO III), treated with rebamipide or not were incubated in the absence or the presence of H. pylori. As a result, H. pylori significantly stimulated IL-S production, which was similar to time course stimulation of lipid peroxidation. Other cytokines (IL-1 alpha, IL-1 beta, IL-6, TNF-alpha) were not stimulated by H. pylori. Treatment with H. pylori resulted in the activation of two species of NF-kappa B dimers (a p50/p65 heterodimer and a p50 homodimer). Rebamipide significantly inhibited lipid peroxidation as an indicative of oxidative damage, NF-kappa B complex formation, and IL-8 production by H. pylori. In conclusion, rebamipide may attenuate H. pylori-induced gastric inflammation by inhibiting lipid peroxidation and oxidant-mediated activation of NF-kappa B and thereby decreasing IL-8 production.