意向性运动干预影响局部脑缺血大鼠GLUA2和N-cadherin表达的影响

目的 研究意向性运动干预治疗对大脑局部缺血大鼠行为学及梗死灶周围组织中GluA2和Ncadherin表达的影响。方法 利用鱼线栓堵法将大鼠制成大脑中动脉栓塞（middle cerebral artery occlusion,MCAO）模型共144只，随机分成模型（MCAO）组、生活环境变化（environment modification,EM）组、普通康复训练（control rehabilitstion, CR）组和意向性运动干预（willed movement,WM）组，每组根据术后时间划分为7 d、15 d、30 d 3个亚组。对各组研究对象的行为变化进行观察分析，通过免疫组化技术研究脑梗死灶周围组织中GluA2和N-cadherin蛋白水平。结果 再灌7 d、15 d、30 d，意向性运动干预组的攀爬频率显著高于EM及CR组（P <0.01）；再灌30 d，和MCAO组相比，意向性运动干预组的神经功能缺损评分更低（P <0.05）；而其缺血半暗带区域GLUA2、N-cadherin蛋白表达量都更高（P <0.05）。结论 对于大脑局部缺血所导致的神经功能障碍...

Effects of Willed Movement on the Expression of GLUA2 and N-cadherin in Rats with Focal Cerebral Ischemia

  Objective  To explore effect of the Willed movement on behaviours of rats with focal cerebral ischemia and the expression of GluA2 and N-cadherin in the brain tissue around ischemia.   Methods  We selected clean-level healthy male SD rats, and prepared 144 middle cerebral artery occlusion （MCAO） models by thread occlusion method, and randomly divided them into model （MCAO） group, environment modification （EM） group, control rehabilitstion （CR） group and Willed movement （WM） group, each group was divided into four subgroups of 7, 15, and 30 days according to the postoperative time. The behavioral changes of rats in each group were dynamically observed, and the expression changes of GluA2 and N-cadherin protein in the brain tissue around the ischemic area were observed by immunohistochemical staining.   Results  On 7, 15, and 30 days after reperfusion, the climbing frequency of rats which were treated by willed movement was obviously higher than EM and CR group （P < 0.01）. After 30 days of reperfusion, the neurological deficits score of the intentional exercise intervention group was lower than MCAO rats （P < 0.05）. Compare with MCAO rats, the expression levels of GLUA2 and N-cadherin were higher in ischemic penumbra （P < 0.05）.   Conclusions  Willed movement can promote the recovery of damaged nerve function after focal cerebral ischemia, which may be related to up-regulating the expression of GLUA2 and N-cadherin in the brain tissue around the ischemic focus and enhancing synaptic plasticity.