Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanism of the inhibitory action of rebamipide, a new mucosal protective drug, was studied using rats with diethyldithiocarbamate-induced gastric antral ulcers. Rebamipide reduced ulcer formation and inhibited the elevation in lipid peroxide concentration in the gastric mucosa. Rebamipide inhibited both luminol- and lucigenin-dependent chemiluminescence of neutrophils activated by formyl-methionyl-leucyl-phenylalanine. Rebamipide did not alter the reduction of cytochrome c induced by the xanthine-xanthine oxidase system or the NADPH-dependent microsomal lipid peroxidation in the liver. These findings suggest that rebamipide prevents diethyldithiocarbamate-induced gastric ulcer formation by inhibiting neutrophil activation.
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PMID:Antiulcer mechanism of action of rebamipide, a novel antiulcer compound, on diethyldithiocarbamate-induced antral gastric ulcers in rats. 131 72

Rebamipide (2-(4-chlorobenzoylamino)-3-[2-(1H)-quinolinon-4-yl] propionic acid), a novel antiulcer agent, has been reported to prevent various acute experimental gastric mucosal lesions and to accelerate the healing of chronic gastric ulcers. We investigated the effect of rebamipide on rat gastric mucosa damaged by exposure to 30 min of ischemia and 60 min of reperfusion (I/R) with continuous intragastric instillation of 0.1 N HCl (1 ml/100 g body weight) into the stomach. Rebamipide, at 30 and 100 mg/kg, i.p., reduced the mucosal damage score from 2.28 (I/R vehicle group) to 1.54 and 1.07, respectively. Pretreatment with rebamipide significantly reduced the activity of myeloperoxidase (an index of neutrophil infiltration) and preserved the activities of superoxide dismutase and nitric oxide synthase in the gastric mucosa with inhibition of malondialdehyde production. Thus, a negative correlation between the activities of nitric oxide synthase and myeloperoxidase (y = 4.35-9.45x, r = .67, P < .01) was observed. In an in vitro study, rebamipide inhibited N-formyl-met-leu-phe-induced chemotaxis of neutrophils and production of superoxide anion from opsonized zymosan-stimulated neutrophils. However, it did not affect the production of superoxide anion either by the xanthine-xanthine oxidase reaction or phorbol 12-myristate 13-acetate-stimulated neutrophils. Based on these results, it is suggested that rebamipide exerts a protective effect on the I/R-induced gastric mucosal damage through inhibition of mobilization and activation of neutrophils in association with an attenuation of the decreases in both superoxide dismutase and nitric oxide synthase activities, thereby preventing the gastric microcirculation from deterioration.
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PMID:Preventive effect of rebamipide on gastric lesions induced by ischemia-reperfusion in the rat. 756 69

Rebamipide, a novel antipeptic ulcer drug, 2-(4-chlorobenzoylamino)-3-[2(1H)-quinolinone-4-yl]-propionic acid, was studied for its inhibitory effect on gastric xanthine oxidase activity and type conversion of the enzyme that has a profound role in free radical generation. Intraperitoneal administration of rebamipide at 60 mg/kg body weight reduced gastric mucosal hemorrhagic lesions and lipid peroxidation, which was proportional to the inhibitory effect of rebamipide on alcohol-induced xanthine oxidase-type conversion and enzyme activity. It was also observed that the activity of xanthine oxidase was significantly inhibited by administration of rebamipide at 60 mg/kg body weight, leading to a significant reduction of lipid peroxide content in alcohol-treated rats. The results suggest that alcohol-induced gastric mucosal lesions might be, in part, due to the increased activity of xanthine oxidase and type conversion rate of the enzyme and the protective effect of rebamipide on gastric mucosal lesions would result from its ability to protect against oxidative stress on gastric mucosal lesions of alcohol-treated rats.
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PMID:The effect of rebamipide on gastric xanthine oxidase activity and type conversion in ethanol-treated rats. 874 82

Helicobacter pylori stimulated human neutrophils to produce oxygen radicals as evidenced by the production of chemiluminescence in the presence of luminol. The capacity of H. pylori to produce oxygen radicals from neutrophils was much higher than that of Escherichia coli and Staphylococcus aureus and is almost as strong as that of PMA. Rebamipide (2-(4-chlorobenzoylamino)-3-[2-(1H)-quinolinon-4-yl] propionic acid) suppressed the chemiluminescence produced by H. pylori-stimulated neutrophils and also suppressed the chemiluminescence produced by a cell-free xanthine/xanthine oxidase reaction with luminol. Thus, it is indicated that this drug has the action of scavenging oxygen radicals. Gastric mucosal cells labelled with a fluorescent dye were damaged by the incubation of the cells with neutrophils and H. pylori, and this damage was protected by rebamipide. The protection of cell damage was ascertained as a decrease in the release of fluorescent dye into the incubation medium and a reduction in the distortion of cell geometry. The data suggest that H. pylori induce human neutrophils to produce oxygen radicals which are responsible for gastric mucosal cell damage and that rebamipide removes the oxygen radicals produced from H. pylori-activated neutrophils and thus reduces the gastric mucosal cell damage. These effects may account for the ulcerogenesis action of H. pylori and for part of the mechanism of the anti-ulcer action of rebamipide.
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PMID:Effects of rebamipide on gastric cell damage by Helicobacter pylori-stimulated human neutrophils. 886 35

Rebamipide, 2-(4-chlorobenzoylamino)-3-[2(1H)-quinolinone-4-yl]-propionic acid, a novel antipeptic ulcer agent, has been reported to prevent various acute experimental gastric mucosal lesions and to accelerate the healing of chronic ulcers. Therapeutic effect of rebamipide was investigated with regard to the inhibitory effect on xanthine oxidase activity and type conversion of the enzyme which play a profound role in oxygen radicals generation system. Intraperitoneal administration of rebamipide at 60 mg/kg body weight reduced the xanthine oxidase activity, lipid peroxide content in ammonia induced hemorrhagic lesion. These results suggest that the therapeutic effect of rebamipide on gastric mucosal lesion may be in part due to the inhibitory activity of xanthine oxidase and type conversion rate of the enzyme.
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PMID:Therapeutic effect of rebamipide on ammonia-induced gastric mucosal hemorrhagic lesion in rats. 987 6