Effects Of Willed Movement Therapy On Expression Of N-cadherin And δ-catenin In Rats Following Ischemic Reperfusion Injury

Object To research the effects of willed movement on the behavior, infarct volume and the protein expression of N-cadherin and8-catenin in cerebral cortex around infarct after ischemic reperfusion injury in rats. Preliminarily explored the possible mechanism of willed movement therapy enhanced synaptic transmission efficiency and brain plasticity, then improved the dysfunction resulted by cerebral ischemia.Methods Transient focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO).One hundred and ninety-two successful model were randomly divided into4groups:MCAO, environment modification (EM), control rehabilitstion (CR) and willed movement (WM).Rats in every group were killed at Neurological and neurobehavioral assessments were performed and the rats were killed at3,7,15and30day recirculation times after120-min period of occlusion of the right middle cerebral artery. TTC staining were used to detected the ischemic lesions volume and immunohistochemistry were used to detected the N-cadherin and δ-catenin protein in cerebral cortex around infarct and analysed the correlativity of two proteins.Results (1)Ethology results showed:rat in WM group have improved more than rats in MCAO group in Neurologic Deficit Score at30day recirculation post-infarction and forelimb test at15,30day recirculation post-infarction.At7,15,30day after cerebral ischemia-reperfusion,the climbing frequency of rats in WM group were significantly higher than those rats in EM group and CR group.(2) TTC staining results showed that the ischemic lesions volume of rats in WM group were bigger than those rats in MCAO group at15day and30day after cerebral ischemia-reperfusion.(3)The results of immunohistoch-emistry showed:the expression of N-cadherin and δ-catenin protein in cerebral cortex around infarct in group WM were significantly increased compared with MCAO group.Conclusions Willed movement therapy promoted motor recovery, the mechanism maybe relate to increasing the expression of N-cadherin and δ-catenin protein in cerebral cortex around infarct.