The mechanism of protective effects of melatonin on global ischemia/reperfusion induced brain injury in rats

SUMMARY Objective: To study the effects of melatonin(MT) on inducible nitric oxide synthase (iNOS) expression in hippocampal CA1 at 24 hours and TDT mediated dUPT nick end labling (TUNEL) positive cells in hippocampal CA1 at 48 hours after global ischemia(20 min)/ reperfusion in rats. Methods: MT was injected intraperitoneally at 0 h, 1 h, 2 h and 6 h after ischemia(20 min) induced by the“occlusion of four arteries”, 2.5 mg·kg -1 or 10 mg·kg -1 each time, respectively. Researching the expression of iNOS in hippocampal CA1 with the immunocytochemistry method 24 hours after reperfusion and the number of TUNEL positive cells in hippocampal CA1 48 hours after reperfusion utilizing TUNEL. Results: At these doses, MT could decrease iNOS expression in hippocampal CA1 at 24 h after global ischemia (20 min)/reperfusion and the number of TUNEL cells in hippocampal CA1 at 48h after reperfusion in rats. Conclusion: Decreasing the expression of deleterious iNOS maybe one of the mechanisms involved in protective action of MT on ischemia vulnerable brain region.