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Role of rebamipide on induction of heat-shock proteins and protection against reactive oxygen metabolite-mediated cell damage in cultured gastric mucosal cells.

Hahm, KB; Park, IS; Kim, YS; Kim, JH; Cho, SW; Lee, SI; Youn, JK
Free radical biology & medicine, 22(4):711-716, 1997
Journal Title
Free radical biology & medicine
Reactive oxygen metabolites (ROM) have been reported to be important in the pathogenesis of ischemia/ reperfusion-, ethanol-, nonsteroidal antiinflammatory drug-, or Helicobacter pylori-induced gastric mucosal injury. Rebamipide, a novel antiulcer agent, has been reported either to prevent various acute experimental gastric mucosal lesions or to accelerate the healing of chronic gastric ulcers. The underlying mechanism by which rebamipide exerts its cytoprotective effect in the damaged stomach is not fully determined. We investigated the role of rebamipide in protecting against ROM-mediated cell damage in gastric mucosal cells and in inducing cytoprotective proteins. Cells were exposed to ROM enzymatically generated by hypoxanthine-xanthine oxidase. Cytotoxicity was quantified by measuring specific 51Cr release from prelabeled cells. ROM caused dose-dependent increase in cytotoxicity and amount of thiobarbituric acid-reactive substances (TBA-RS). ROM-induced cytotoxicity and TBA-RS were dose-dependently decreased by the addition of rebamipide and/or catalase, but not by superoxide dismutase alone. The effects of rebamipide on electric spin resonance signal were investigated. We found that the DMPO spin adduct ESR signal of hydroxyl radicals (DMPO-OH) was significantly attenuated by rebamipide. Western blot analysis showed that induction of heat-shock protein (HSP70) was significantly increased following rebamipide administration in a dose-dependent manner. Based on these results, it is concluded that rebamipide exerted a protective effect on HX-XO-induced gastric mucosal cell cytotoxicity through one or more of the following mechanism(s): (1) inhibition of lipid peroxidation of the cell membrane; (2) hydroxyl radical scavenging activity; and (3) induction of cellular cytoprotective protein such as HSP70.
MeSH terms
Alanine/*analogs & derivatives/pharmacologyAnimalsAnti-Ulcer Agents/pharmacologyCatalase/pharmacologyCell Death/drug effectsCells, CulturedFree Radical Scavengers/pharmacologyGastric Mucosa/*drug effects/injuries/*metabolismHSP70 Heat-Shock Proteins/*biosynthesisHydroxyl Radical/metabolismHypoxanthine/toxicityLipid Peroxidation/drug effectsQuinolones/*pharmacologyRabbitsReactive Oxygen Species/*metabolismSuperoxide Dismutase/pharmacologyThiobarbituric Acid Reactive Substances/metabolismXanthine Oxidase/toxicity
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
Journal Papers > School of Medicine / Graduate School of Medicine > Gastroenterology
AJOU Authors
함, 기백김, 영수김, 진홍조, 성원윤, 정구
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