麻黄碱促进脑缺血大鼠运动功能康复的细胞及分子机制

目的:研究麻黄碱加速大鼠大脑中动脉闭塞(MCAO)模型运动功能康复的细胞和分子机制. 方法: 雄性SD大鼠60只,随机分为假手术组、自然康复组和治疗组. 应用线栓法建立单侧MCAO模型. 术后1,2,3,4 wk电镜检测缺血周围区组织损伤及新生突触形成情况,RT-PCR检测缺血周围区生长相关蛋白(GAP-43), 突触素(SYP)表达的变化. 结果: 治疗组神经损伤程度轻,新生突触较自然康复组多;RT-PCR显示治疗组GAP-43和SYP的表达水平高于自然康复组(P＜0.01). 结论: 增加缺血周围区新生突触形成,在基因水平上促进GAP-43及SYP的表达增高是麻黄碱促进神经康复的机制之一.

Effect of ephedrine on motor recovery after brain ischemia in rats and its cellular and molecular mechanisms

AIM: To investigate the effect of ephedrine on motor recovery after middle cerebral artery occlusion (MCAO), and explore the molecular and cellular mechanisms of ephedrine in accelerating rehabilitation in rats. METHODS: Sixty male SD rats were randomly divided into sham-operated group, natural recovery group and ephedrine treatment group. The unilateral MCAO models were induced by using bread occlusion method. Electron microscope was used to observe the tissue damages and newly born synapses around ischemic area at week 1, 2, 3 and 4 after operation. The expression levels of growth-associated protein 43 (GAP-43) and synaptophysin around ischemic area were exa-mined by RT-PCR techniques. RESULTS: The ephedrine treatment group was lighter in degree of injury and more in the number of newly born synapses as compared with the natural recovery group. Both GAP-43 and synaptophysin proteins were demons-trated statistically significantly increased in RT-PCR product as determined by optical density measurements in ephedrine treatment group as compared with natural recovery group (P<0.01). CONCLUSION: The mechanisms of behavioral recovery with ephedrine treatment are associated with the enhanced synaptoge-nesis and the increased expression of molecules involved in neuronal remodeling around ischemic area.