Natural plant origin products like amygdalin with anti-inflammatory effects are still a major part of traditional medicine. We conducted the present investigation to elucidate the amygdalin effects on alcohol-induced gastric ulcer together with the possible role of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-α). Thirty-two male Wistar rats were used to study therapeutic and preventive effects of amygdalin on absolute alcohol-induced gastric ulcer. Animals were equally divided into 4 groups (n=8): (I) control, (II) Alcohol; absolute alcohol (1 ml/200 g b.w) used to induce gastric ulcer, (III) Alcohol/Amygda; amygdalin (2 mg/kg/day intramuscular) administrated for three weeks after gastric ulcer induction and (IV) Amygda/Alcohol; amygdalin was given for three weeks before gastric ulcer induction. Ulcer index, gastric acid secretion, gastric tissue’s NO metabolites andTNF-α level measured. Ulcer index was significantly decreased in Alcohol/Amygda than Alcohol group (p<0.05). Gastric tissue’s NO metabolites level and gastric acid secretion decreased in Alcohol and Amygda/Alcohol groups than control (p<0.05). Gastric tissue TNF-α level increased in Alcohol and Amygda/Alcohol rats than control group (p<0.05). The results of this study show that amygdalin protected gastric mucosa from alcohol-induced gastric ulcer. This gastroprotection may mediate via gastric mucosal nitric oxide production and TNF-α suppression.
Key words: Amygdalin, gastric ulcer, nitric oxide, TNF-α.
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