L-arginine protects against ethylene glycol-induced gastric mucosal damage in rats: immunohistochemical and electron microscopic study
Ethylene glycol is an alcohol widely used in industry as an antifreeze. It affects the normal gastric mucosal defense mechanisms, inducing surface ulcerations. L-arginine is a precursor of nitric oxide that exhibits multiple biological properties; among them is the acceleration of wound healing, especially in the stomach. Caspase-3 immunohistochemistry, and semithin and ultrathin section examinations were used to investigate the possible protective effect of L-arginine on ethylene glycol-induced gastric mucosal damage in rats. Three animal groups were used: group A (control group), group B (received 3.3 mL/kg ethylene glycol for 2 weeks), and group C (received 200 mg/kg of L-arginine and 3.3 mL/kg ethylene glycol for 2 weeks). By examination, group B showed significant increases in caspase-3 positive cells in comparison to the control, semithin sections revealed surface disruption and ulcerations, and ultrathin sections showed multiple pathological changes in cells lining the gastric mucosal glands. In group C significant decreases in caspase-3 positive cells were encountered and the other pathological findings in group B were found to be reversed. Therefore, we conclude that ethylene glycol-induced damage to the gastric mucosa could be prevented by L-arginine administration.
L-arginine protects against ethylene glycol-induced gastric mucosal damage in rats: immunohistochemical and electron microscopic study
Ethylene glycol is an alcohol widely used in industry as an antifreeze. It affects the normal gastric mucosal defense mechanisms, inducing surface ulcerations. L-arginine is a precursor of nitric oxide that exhibits multiple biological properties; among them is the acceleration of wound healing, especially in the stomach. Caspase-3 immunohistochemistry, and semithin and ultrathin section examinations were used to investigate the possible protective effect of L-arginine on ethylene glycol-induced gastric mucosal damage in rats. Three animal groups were used: group A (control group), group B (received 3.3 mL/kg ethylene glycol for 2 weeks), and group C (received 200 mg/kg of L-arginine and 3.3 mL/kg ethylene glycol for 2 weeks). By examination, group B showed significant increases in caspase-3 positive cells in comparison to the control, semithin sections revealed surface disruption and ulcerations, and ultrathin sections showed multiple pathological changes in cells lining the gastric mucosal glands. In group C significant decreases in caspase-3 positive cells were encountered and the other pathological findings in group B were found to be reversed. Therefore, we conclude that ethylene glycol-induced damage to the gastric mucosa could be prevented by L-arginine administration.
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