Abstract: AIM: To investigate the effects of melatonin on gastric lesions and mucosal nuclear factor-κB (NF-κB) activation in rats with stress ulcer for elucidating the molecular mechanisms of melatonin intervention in vivo. METHODS: Stress ulcer was induced by water-immersion restraint (WIR) stress for 6 h.Melatonin (5 and 20 mg°kg^-1, ip) was administrated 30 min before WIR stress.After 6 h of WIR, rats were killed and the stomachs were removed.Ulcer index (UI) was used for evaluated macroscopic injury and gastric mucosal MDA contents and NF-κB activation were determined.RESULTS: Severe gastric lesions were induced after WIR stress for 6 h. There was a significantly increased in MDA contents (P<0.01) and NF-κB activation (P<0.01) in gastric mucosal in stress group.The gastric lesions in MT 5 mg°kg^-1 group and 20 mg°kg^-1 group were significantly relieved than that in the stress group after 30 min administration of melatonin (P<0.01).The UI (P<0.05) and mucosal MDA contents (P<0.01) in MT 20 mg°kg^-1 group were significantly lower than that in MT 5 mg°kg^-1 group.But there was no significantly difference in mucosal NF-κB activity between two groups.CONCLUSION: Melatonin can prevent the development of stress ulcer via a mechanism involving in reducing oxidative stress-induced NF-κB activation in gastric mucosa.

Key words: melatonin, stress ulcer, nuclear factor-κB, gastric mucosal