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Non-steroidal anti-inflammatory drugs(NSAIDs) induce tissue damage and oxidative stress in animal models of stomach damage. In the present study, the protective effects of wheat peptides were evaluated in a NSAID-induced stomach damage model in rats. Different doses of wheat peptides or distilled water were administered daily by gavage for 30 days before the rat stomach damage model was established by administration of NSAIDs(aspirin and indomethacin) into the digestive tract twice. The treatment of wheat peptides decreased the NSAID-induced gastric epithelial cell degeneration and oxidative stress and NO levels in the rats. Wheat peptides significantly increased the superoxide dismutase(SOD) and glutathione peroxidase(GPx) activities and decreased i NOS activity in stomach. The m RNA expression level of μ-opioid receptor was significantly decreased in wheat peptides-treated rats than that in in the control rats. The results suggest that NSAID drugs induced stomach damage in rats, wchih can be prevented by wheat peptides. The mechanisms for the protective effects were most likely through reducing NSAID-induced oxidative stress.
In the present study, the protective effects of wheat peptides were evaluated in a NSAID-induced stomach damage model in rats. Different doses of wheat peptides or distilled water were administered daily by gavage for 30 days before the rat stomach damage model was established by administration of NSAIDs (aspirin and indomethacin) into the digestive tract twice. The treatment of wheat peptides decreased the NSAID-induced gastric epithelial cell degeneration and oxidative stress and NO levels in the rats. Wheat mins significantly increased the superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and decreased i NOS activity in stomach. The m RNA expression level of μ-opioid receptor was significantly decreased in wheat peptides-treated rats than that in the control rats. The results suggest that NSAID drugs induced stomach damage in rats, wch The mechanisms for the protective effects were most likely through reducing NSAID-induced oxidative stress.