Abstract: Objective C57black/6 mice are increasingly used for experimental stroke research while how the neuron death is induced and what the pathway of dead signal transduction is after ischemia in this model are still unknown.Methods In this study global cerebral ischemia was induced by bilateral common carotid artery occlusion(BCCAO) in C57black6 mice.C57black/6 mice were subjected to 15 min occlusion followed by reperfusion for 24 h.Fas-L and Caspase-3 immunohistochemical staining of brain tissue were performed. Results Fas-L-positive neurons were distributed in retrosplenial agranular cortex(RSA),piriform cortex(Pir),ventral posterolateral thalamic nucleus/ventral posteromedial thalamic nucleus(VPL/VPM),arcuate hypothalamic nucleus(Arc) and medial amygdaloid nucleus,posteroventral(MePV) areas and the cytoplasm was stained.There were more positive neurons in the ischemia group than in the sham-surgery group(P<0.01) for all observed areas except VPL/VPM.And the positive neurons were more darkly stained in the ischemia group(P<0.01).Caspase-3-positive neurons were distributed in RSA,Pir,VPL/VPM and MePV areas.The Caspase-3-positive neurons were less in number and lightly stained compared with Fas-L-positive neurons.Also there were more Caspase-3-positive neurons in the ischemia group than in the sham-surgery group(P<(0.05),P<0.01).The positive neurons were more darkly stained in the ischemia group(P<0.01).Conclusion These results showed that C57black/6 mice model of global ischemia can induce extensive expression of Fas-L and Caspase-3 in brain,indicating that members of Caspases family were involved in the pathway of neuron death signal transduction and there was exogenetic pathway during this process for this kind of global ischemia model.

Key words: C57black/6 mice, global cerebral ischemia, Fas-L, Caspase-3