Effects of Rebamipide, a Novel Anti-Ulcer Agent, on Gastric Mucosal Injury Induced by Platelet-Activating Factor in Rats

We examined the role of gastric mucosal bloodflow, lipid peroxidation, and neutrophil accumulationmediated by platelet-activating factor in the protectiveeffect of rebamipide against gastric mucosal injury in rats. The intravenous injection ofplatelet-activating factor induced hyperemia andhemorrhagic erosions in rat stomachs. Rebamipide did notaffect the decrease in the gastric mucosal blood flow induced by platelet-activating factor. Theincrease in gastric injury score afterplatelet-activating factor injection and the increase inthiobarbituric acid-reactive substances weresignificantly inhibited by the administration of rebamipide. Thegastric injury score was closely correlated with theaccumulation of lipid peroxides. Tissue-associatedmyeloperoxidase activity in the gastric mucosasignificantly increased after platelet activating factorinjection; this increase was not influenced byrebamipide treatment. The protective effect ofrebamipide against the platelet-activitingfactor-induced gastric mucosal injury may be due to direct inhibitionof lipid peroxidation or scavenging of oxygen radicalsthat initiate lipid peroxidation.