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Inhibition of Ethanol-Induced Gastric Mucosal Damage by Carvedilol in Male Wistar Albino Rats: Possible Biochemical Changes

Keywords: Carvedilol , gastric secretions , nucleic-acids , sulfhydryls , lipid-peroxides , ulceration , glutathione

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The effect of acute carvedilol (a third-generation nonselective β-blocker) pretreatment on gastric mucosal injury induced by 80% ethanol was investigated in male Wistar albino rats. The effects caused by pylorous ligation, accumulated gastric acid secretions and ethanol-induced changes in gastric mucus secretions, levels of proteins, nucleic acid, malondialdehyde (MDA) and non-protein sulfhydryl groups (NP-SH) in the stomach wall were investigated. The gastric ulcers were induced by administration of 1 mL of 80% ethanol, as a necrotizing agent into the stomach. Carvedilol pretreatment at two oral doses of 30 and 60 mg kg-1 body weight were found to protect against the ulcerogenic effects of ethanol. Same dose regimen of carvedilol offered significant protection against ethanol-induced damage on the parameters evaluated for histopathology. Furthermore, the pretreatment afforded a significant inhibition of pylorous ligated accumulation of gastric acid secretions and ethanol-induced depletion of stomach wall mucus, nucleic acids, proteins and NP-SH contents. Only higher dose of carvedilol provided inhibition of ethanol-induced increase in MDA concentration. The protective effects of carvedilol against gastric secretion or damage to the gastric-wall mucosa may be mediated through its effects on mucus production and NP-SH concentrations, possible free-radical scavenging ability and/or cytoprotective properties.


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