血管性痴呆大鼠海马超微结构的变化及药物干预

Drug intervention on ultrastructural changes of hippocampus in vascular dementia rats

目的:探讨血管性痴呆病理机制及黄精口服液的作用机制。方法:结扎双侧颈总动脉建立血管性痴呆模型,黄精口服液灌胃,应用透射电镜观测神经细胞、胶质细胞、微血管病理变化和突触结构参数的变化。结果:血管性痴呆大鼠海马CA1区神经组织线粒体肿胀、嵴断裂、模糊或消失,微管断裂、排列紊乱,神经毡中突起肿胀、变性,突触结构参数明显改变;毛细血管内皮细胞局部基膜和星形胶质细胞也有病理改变。黄精口服液干预的大鼠海马组织病理变化明显减轻;海马CA1突触界面曲率增大、突触后致密物增厚、突触活性区增长。结论:(1)突触结构变化是血管性痴呆的病理机制之一;(2)黄精口服液促进突触重建、改善血管性痴呆大鼠学习记忆能力。

Objective: To explore the neuropathological mechanism of vascular dementia and the effect of extract polygonatum by observing the ultrastructural changes of hippocampus in rats with vascular dementia (VD). Methods: Rat VD models established by permanent occlusion of the bilateral common carotid artery were challenged with Morris water maze to assess their learning and memory ability. The change of the hippocampal tissue was studied with transmission electron microscope and morphometric analysis. Results: The swollen and disrupted mitochondria, disarranged microtubule and degenerated neuropil were frequently found in the hippocampal CA1 area of vascular dementia rats. The capillaries displayed irregular thickening and split basement membranes. Deposits were seen in the basement membrane in some dementia rats. There were myelin-like materials outside of some basement membrances, which was not present in the control animals. There was widespread accumulation of lipofuscin in glial cells and pericytes. The curvature of synaptic interface, the thickness of postsynaptic density and the length of synaptic active zone were increased in rats treated with polygonatum oral liquid. Conclusion: Treatment of extract polygonatum may improve synaptic remodelling and promote learning and memory in rats with vascular dementia.