基于突触可塑性探讨电针改善大脑中动脉闭塞大鼠运动障碍的作用机制

Mechanism of Electroacupuncture in Improving Dyskinesia in MCAO Rats Based on Synaptic Plasticity

目的:基于突触可塑性观察电针曲池、足三里对大脑中动脉闭塞(MCAO)大鼠运动障碍的改善。方法:将60只雄性SD大鼠随机分为假手术组、模型组、穴位组、非穴组,每组15只。采用Zea Longa线拴法制备MCAO大鼠模型,电针曲池、足三里,干预14 d。通过神经功能评分判断大鼠的神经功能缺损情况;CatWalk步态分析比较各组大鼠运动功能,TTC染色观察脑梗死体积,透射电镜观察突触超微结构和数量,免疫荧光检测缺血侧运动皮层突触相关因子突触后致密物-95(PSD-95)、突触蛋白的表达情况。结果:干预14 d后,与模型组比较,穴位组大鼠神经功能评分降低(P<0.05);步行速度提高、双足支撑时间缩短(P<0.05);脑梗死体积减少(P<0.05);突触超微结构改善明显,突触数量增加(P<0.05),突触相关因子突触蛋白、PSD-95表达上调(P<0.05)。Catwalk步态参数、脑梗死体积与突触超微结构改善有一致性。结论:电针曲池、足三里穴可改善MCAO大鼠运动障碍,其机制可能与上调突触相关因子的表达,改善突触可塑性有关。

Objective:To observe the effect of electroacupuncture(EA)at“Quchi(LI 11)”and“Zusanli(ST 36)”on the dyskinesia in middle cerebral artery occlusion(MCAO)rats based on synaptic plasticity.Methods:Sixty male SD rats were randomly divided into a sham operation group,a model group,an acupoint group,and a non-acupoint group,with 15 rats in each group.The MCAO model was induced in rats by the Zea-Longa method.EA treatment at“Quchi(LI 11)”and“Zusanli(ST 36)”was carried out for 14 days.The neurological deficits of rats were evaluated by the score of the Neurological Impairment Scale.The motor functions of rats in each group were compared by the CatWalk-assisted gait analysis system.TTC staining was used to observe the cerebral infarction volume.The ultrastructure and number of synapses were observed by transmission electron microscopy(TEM).The expression of synapse-related factors PSD-95 and synapsin in the ischemic motor cortex was detected by immunofluorescence assay.Results:After 14 days of intervention,compared with the model group,the acupoint group showed decreased neurological deficit score(P<0.05),quickened walking,shortened bipedal stance time(P<0.05),reduced cerebral infarction volume(P<0.05),improved synapse ultrastructure,increased number of synapses(P<0.05),and up-regulated expression of synapse-related factors synapsin and PSD-95(P<0.05).Catwalk gait parameters and cerebral infarction volume were consistent with synaptic ultrastructure improvement.Conclusion:EA at“Quchi(LI 11)”and“Zusanli(ST 36)”can improve dyskinesia in MCAO rats,and the mechanism may be related to the up-regulation of the expression of synaptic-related factors and the improvement of synaptic plasticity.