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中文摘要：
目的考察文冠果壳苷对大鼠大脑中动脉缺血再灌注损伤的改善作用,并从改善突触功能的角度,探讨其作用机制。方法利用大脑中动脉阻塞法（MCAO）制备大鼠局灶性脑缺血再灌注损伤模型,TTC染色法计算脑梗死面积,HE染色法观察海马CA1区神经细胞病理形态改变,透射电镜观察大脑皮层缺血半暗带区神经元及突触超微结构改变,Western blotting检测突触相关蛋白SYP、PSD95及GAP43的表达。结果文冠果壳苷显著改善模型大鼠神经功能缺失症状,减少脑梗死面积,改善海马CA1区神经细胞的病理改变,并改善脑缺血半暗带区神经元及突触超微结构的损伤,增加突触相关蛋白SYP、PSD95及GAP43的表达。结论文冠果壳苷可显著改善大鼠大脑中动脉缺血再灌注损伤,其机制可能与促进突触重塑和/或减轻突触结构与功能的损伤有关。
英文摘要：
Objective To investigate the effects and the preliminary mechanism of xanthoceraside on the focal cerebral ischemia-reperfusion injury. Methods Middle cerebral artery occlusion （ MACO ） was used to obtain the focal cerebral ischemia-repeffusion injury model;HE staining was used for the pathomorphology study; transmission electron microscope was used to observe the ultra-structure of the neurons and synapses; western blotting was used to detect the expression of synaptic related proteins. Results Xanthoceraside significantly increased the neurological scores and decreased the infract area of brain in model rats. It improved the patho- morphological changes in hippocampus CA1 region and the ultra-structure changes of neuronal nuclear and synapses in the ischemic penumbra of model rats;meanwhile it increased the expression of synaptic related protein in ischemic penumbra of rats. Conclusions The synaptic regeneration and/or the improvement of synaptic structure and function mingt be associated with the alleviating effect of xanthoceraside to the focal cerebral ischemia-reperfusion injury.
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