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Inhibition of Lipid Peroxidation, NF-κB Activation and IL-8 Production by Rebamipide in Helicobacter pylori-Stimulated Gastric Epithelial Cells

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Abstract

The present study aimed to investigate whether rebamipide, a novel antiulcer agent that has an oxygen radical scavenging activity, would inhibit lipid peroxidation, NF-κB 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-8 production, which was similar to time course stimulation of lipid peroxidation. Other cytokines (IL-1α, IL-1β, IL-6, TNF-α) were not stimulated by H. pylori. Treatment with H. pylori resulted in the activation of two species of NF-κB dimers (a p50/p65 heterodimer and a p50 homodimer). Rebamipide significantly inhibited lipid peroxidation as an indicative of oxidative damage, NF-κB 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-κB and thereby decreasing IL-8 production.

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Kim, H., Seo, J.Y. & Kim, K.H. Inhibition of Lipid Peroxidation, NF-κB Activation and IL-8 Production by Rebamipide in Helicobacter pylori-Stimulated Gastric Epithelial Cells. Dig Dis Sci 45, 621–628 (2000). https://doi.org/10.1023/A:1005474013988

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