Temporospatial Alterations of Activation of Extracellar Signal-regulated Kinases in Cortex Involved in the Injury of Cerebral Ischemia
Linfang Li
Abstract
Linfang Li
Abstract
Objective To investigate the temporospatial alterations and effect of the activation of extracellular signal-regulated kinase 1(ERK1)in perifocal cortex involved in cerebral ischemic injury.Methods The cerebral ischemia focally 2 h and reperfusion 72 h model in rabbits was induced by transient occlusion of middle cerebral artery(MCA).Here the dynamic changes of expression of ERK1 in perifocal cortex of the rabbit brain exposed to 2 h ischemia and different periods of reperfusion were detected by immunohistochemistry.Meantime,the apoptosis status were detected by immunohistochemistry and by flow cytometry methods.Results ERK1 activation was first increased in perifocal cortex at 1 h of reperfusion and strongly activated at 6 h with a peak at 3 d by immuohistochemistry,and gradually decreased to basal level at 14 d of reperfusion(0.22±0.02,0.25±0.02,0.42±0.04,0.14±0.02).All these were correlated with the change of apoptosis in the perifocal cortex.Conclusions ERK signaling pathway was involved in the ischemic injury and played an important role in apoptosis of neurons and focally cerebral ischemia,this finding may provide a therapeutic apporach for cerebral ischemia.
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Objective To investigate the temporospatial alterations and effect of the activation of extracellular signal-regulated kinase 1(ERK1)in perifocal cortex involved in cerebral ischemic injury.Methods The cerebral ischemia focally 2 h and reperfusion 72 h model in rabbits was induced by transient occlusion of middle cerebral artery(MCA).Here the dynamic changes of expression of ERK1 in perifocal cortex of the rabbit brain exposed to 2 h ischemia and different periods of reperfusion were detected by immunohistochemistry.Meantime,the apoptosis status were detected by immunohistochemistry and by flow cytometry methods.Results ERK1 activation was first increased in perifocal cortex at 1 h of reperfusion and strongly activated at 6 h with a peak at 3 d by immuohistochemistry,and gradually decreased to basal level at 14 d of reperfusion(0.22±0.02,0.25±0.02,0.42±0.04,0.14±0.02).All these were correlated with the change of apoptosis in the perifocal cortex.Conclusions ERK signaling pathway was involved in the ischemic injury and played an important role in apoptosis of neurons and focally cerebral ischemia,this finding may provide a therapeutic apporach for cerebral ischemia.
Key concepts: Ischemia, Cerebral cortex, Cortex (anatomy), MAPK/ERK pathway, Immunohistochemistry, Kinase, Apoptosis, Middle cerebral artery