H. Kim et al., Inhibition of lipid peroxidation, NF-kappa B activation and IL-8 production by rebamipide in Helicobacter pylori-stimulated gastric epithelial cells, DIG DIS SCI, 45(3), 2000, pp. 621-628
The present study aimed to investigate whether rebamipide, a novel antiulce
r agent that has an oxygen radical scavenging activity, would inhibit lipid
peroxidation, NF-kappa B activation, and IL-8 production by H. pylori. Hum
an 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 wi
th H. pylori resulted in the activation of two species of NF-kappa B dimers
(a p50/p65 heterodimer and a p50 homodimer). Rebamipide significantly inhi
bited lipid peroxidation as an indicative of oxidative damage, NF-kappa B c
omplex formation, and IL-8 production by H. pylori. In conclusion, rebamipi
de may attenuate H. pylori-induced gastric inflammation by inhibiting lipid
peroxidation and oxidant-mediated activation of NF-kappa B and thereby dec
reasing IL-8 production.