早期“强制性使用”运动疗法对局灶性脑梗死大鼠行为学评分及神经生长因子的影响

Effects of early constraint-induced movement therapy for the grade of behavior and expression of NGF on focal cerebral infarction rats

目的:探讨脑卒中后早期强制性使用单侧肢体对局灶性脑梗死大鼠行为学评分及大脑皮质梗死周围(NGF)表达的影响。方法:健康雄性Sprague-Dawley(SD)大鼠,用大鼠大脑中动脉线栓法(MCAO)建立永久性缺血模型,按照Zea-Longa的方法对动物的行为缺陷进行评分,选取1—3分者60只,将60只大鼠随机分为2组,健侧前肢固定组(A组)30只,未固定组(B组)30只,7d时解除固定,再采用随机区组法分为14d时处死组和21d处死组,各组动物在7d时和处死前做神经功能评分(Longa评分),采用免疫组织化学(SP)方法观察NGF蛋白的表达;采用(POD法)原位杂交方法检测NGF mRNA表达。结果:固定组与未固定组相比,早期“强制性使用”运动疗法可以改善14d及21d的行为学评分,有显著性意义(P<0.05);在梗死周围皮质NGF蛋白和NGF mRNA的表达,固定组14d时表达均明显高于非固定组(P<0.05),而在21d时无显著性意义。结论:早期“强制性使用”运动疗法可以改善神经功能的恢复,从基因水平来提高NGF的表达可能为其发挥作用的机制之一。

Objective： To study the effects of early constraint-induced movement therapy for the grade of behavior of focal cerebral infarction rats and expression of NGF in the peripheral around infarction. Method： Healthy male Sprague-Dawley rats, model with cerebral infarction was established according to Zea-Longa by bloeking middle cerebral artery （MCA） with a nylon thread.Following middle cerebral artery occlusion （MCAO） with 1-3 grading according to Longa, the rats were randomly divided into two groups： constraint-induced movement therapy group（A group,30） and non constraint-induced movement therapy group （B group,30）. Relieved fixation at 7th day. Then divided into 14th and 21st day execution at random. All rats were evaluated the behavior scores in the 7th day and before sacrificing and the samples were processed by immunohistochemistry to evaluate effects of NGF expression, hybridization in situ to evaluate effects of NGF mRNA expression. Result： Comparing with the control group（group B）, constraint-induced movement therapy group（group A） can improve the behavior on the 14th day and 21st day（P〈0.05） and there was a significant up-regulation of the expression of NGF and NGF mRNA（P〈0.05） in the peripheral tissue around infarction on 14th day, but was not significant improved on 21st day （P〉0.05）. Conclusion： Constraint-induced movement therapy may up-regulate of the expression of NGF in genetic transcription level to protect the infarction injury.