Relationship of Expression of Nogo-A Protein and GAP-43 Gene with Nerve Regeneration after Cerebral Ischemia/Reperfusion Injury in Rats
Dong Zheng-min
Abstract
Dong Zheng-min
Abstract
Objective:To investigate the relationship between the expression of Nogo-A protein and growth-associated protein (GAP)-43 gene with nerve regeneration after cerebral ischemia/reperfusion injury in rats. Methods:The healthy adult male Wister rats (162) were randomly divided into TUNEL group,Nogo-A group and GAP-43 group (n=54 each),and they were subdivided randomly into sham-operation group (A) and ischemia-1 h/reperfusion 2 h,6 h,12 h,24 h,48 h,3 day,7 day,14 day groups (n=6,each). By using improved thread occlusion method,the models of intraluminal middle cerebral artery occlusion (MCAO) and reperfusion were induced. Immunohistochemistry was used to detect the apoptosis of neurons,and the expression of Nogo-A protein and GAP-43 mRNA in hippocampus,cortical area and striatal area,and observe the changes in dynamic state of neurons regeneration and infarct focus repair in cerebral ischemic penumbra. Results:There were few apoptostic neurons and weak expression of Nogo-A protein and GAP-43 mRNA in hippocampus,cortical area and striatal area in sham-operation group. In ischemia/reperfusion group,the number of positive cells and expression levels were began to significantly increase at the 2nd h,reached the peak at the 3rd day,and at the 14th day,the number of apoptostic cells was significantly reduced,the expression of Nogo-A protein reached the lowest,and GAP-43 mRNA was weakly expressed (P0.05). Conclusion:The expression of Nogo-A protein can inhibit neuron axon regeneration,and that of GAP-43 mRNA can promote neural plasticity regeneration.
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Objective:To investigate the relationship between the expression of Nogo-A protein and growth-associated protein (GAP)-43 gene with nerve regeneration after cerebral ischemia/reperfusion injury in rats. Methods:The healthy adult male Wister rats (162) were randomly divided into TUNEL group,Nogo-A group and GAP-43 group (n=54 each),and they were subdivided randomly into sham-operation group (A) and ischemia-1 h/reperfusion 2 h,6 h,12 h,24 h,48 h,3 day,7 day,14 day groups (n=6,each). By using improved thread occlusion method,the models of intraluminal middle cerebral artery occlusion (MCAO) and reperfusion were induced. Immunohistochemistry was used to detect the apoptosis of neurons,and the expression of Nogo-A protein and GAP-43 mRNA in hippocampus,cortical area and striatal area,and observe the changes in dynamic state of neurons regeneration and infarct focus repair in cerebral ischemic penumbra. Results:There were few apoptostic neurons and weak expression of Nogo-A protein and GAP-43 mRNA in hippocampus,cortical area and striatal area in sham-operation group. In ischemia/reperfusion group,the number of positive cells and expression levels were began to significantly increase at the 2nd h,reached the peak at the 3rd day,and at the 14th day,the number of apoptostic cells was significantly reduced,the expression of Nogo-A protein reached the lowest,and GAP-43 mRNA was weakly expressed (P0.05). Conclusion:The expression of Nogo-A protein can inhibit neuron axon regeneration,and that of GAP-43 mRNA can promote neural plasticity regeneration.
Key concepts: Penumbra, Gap-43 protein, Ischemia, Axon, TUNEL assay, Apoptosis, Regeneration (biology), Messenger RNA