Abstract: AIM: To observe apoptosis of the neurocytes after focal cerebral ischemia-reperfusion injury (CIRI) in the brain tissue of rats and the effects and mechanism of melatonin (MT).METHODS: The models with cerebral ischemicre-reperfusion were induced by intraluminal middle cerebral artery occlusion (MCAO) with a nylon monofilament suture, 2 h occlusion followed by 24 h reperfusion.MT was intraperitonealed after reperfusion for 0, 1, 2, 6 h.The volume of cerbral infarction was observed using 2, 3, 4-triphenyl tetrazolium chloride (TTC) dyeing, apoptosis of the neurocytes was detected with TUNEL technique, the expression levels of Bcl-2 and Bax proteinum in brain tissue were detected by immunohistochemistry technique, the calcineurin activation in brain tissue was determined by inorganic phosphate method, ATP contents in brain tissue were measured with capillary zone electrophoresis(CZE) method.RESULTS: Compared with the vehicle model, the volume of cerbral infarction was reduced significantly by 10, 20 mg/kg MT, apoptosis of the neurocytes of ischemia penumbra (IP) area in the brain tissue was depressed by 20 mg/kg MT, the ratio of Bcl-2/Bax proteinum expression was increased, and the calcineurin activation of brain tissue in injured side was inhibited significantly, ATP contents in brain tissue were advanced.CONCLUSION: MT can antagonize apoptosis of the neurocytes in brain tissue after CIRI, reduce the volume of cerbral infarction.The mechanism may be related with the ratio of up-regulation Bcl-2/Bax, advancing of calcineurin activation inhibition, increasing of the ATP capacity.

Key words: cerebral ischemia-reperfusion injury, melatonin, apoptosis, Bcl-2/Bax, calcineurin, ATP