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.
Bibliographical noteFunding Information:
Manuscript received January 29, 1999; accepted August 26, 1999. From the Department of Pharmacology and Institute of Gastroenterology, Yonsei University College of Medicine, Seoul 120-752, Korea. This study was supported by a grant from the Korea Otsuka Pharmaceutical Co., Ltd., Seoul, Korea. Address for reprint requests: Dr. Kyung Hwan Kim, Department of Pharmacology, Yonsei University College of Medicine, Seoul 120-752, Korea.
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