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.