高脂血症大鼠模型脑组织病理分析

Pathological Analysis of Brain Tissues of Hyperlipidemia Rat Model

目的:围绕神经-血管单元及脑缺血性损伤相关因素,分析高脂血症大鼠模型脑组织的病理性变化,为研究高脂血症并发脑缺血模型提供理论依据。方法:建立高脂血症及高脂血症合并脑缺血大鼠模型,用ELISA法测大鼠血清NO、ET-1、PGI2、TX-A2、MCP-1、TNF-α和CRP等因子,观察高脂血症模型血管及内皮细胞变化和炎症反应状态;通过病理形态学观察,比较高脂血症神经元、小血管、神经胶质细胞等结构特点;电镜观察神经元亚结构改变。结果:高脂血症模型与正常模型比较,NO、PGI2、TX-A2、MCP-1、TNF-α、CRP表达情况均有显著性差异;大脑皮质可见较多神经细胞和胶质细胞,毛细血管明显增多,海马区有大量的神经细胞但明显萎缩;神经元和小动脉线粒体嵴变短或消失,嵴间腔扩大;粗面内质网扩张,核糖体部分脱离;神经突触的突触小泡减少,线粒体嵴少数变短。结论:与脑缺血损伤相关因素在高脂血症大鼠模型组织中也发生了改变,并对神经元产生一定影响;高脂血症并发脑缺血后,这些因素是否起协同效应值得进一步深入研究;建立高脂血症并发脑缺血模型,应有统一、规范的标准。

Objective： To analyze the pathological changes of brain tissue of hyperlipidemia rat model according to the nerve-vas- cular units and related factors to ischemic brain injury., and to provide theoretical basis for tile study of hyperlipidemia complicat- ed with cerebral ischemia models. Methods ： Hyperlipidemia rat models and hyperlipidemia complicated with cerebral ischemia rat models were established to measure the serum NO, ET - 1, PGI2, TX - A2 , MCP - 1, TNF -αand CRP factors with ELISA method, and to observe the changes of vessels and endothelial cells of hyperlipidemia models ; and its itrflammatory status ; struc- tural features of neurons, small blood vessels and glial cells of hyperlipidemia rats were compared with morphological observation; the neuronal subpopulations structure changes were observed with electron microscope. Results ： The expressions of NO, PGI2 , TX - A2 , MCP - t, TNF -α, CRP of hyperlipidemia models were significantly different from that of the normal models ; there were more neurons and gila] cells in the cerebral cortex, the capillaries increased significantly, there was a large number of nerve cells in the hippocampus but they withered significantly; neurons and arteriolar mitochondrial cristae became shorter or disap- peared, crest cavity expanded ; rough endoplasmic reticulum expanded and parts of the ribosomes broke away ; the neural synaptic vesicles reduced and a few mitochondria became shorter. Conclusion： The relevant factors leading to cerebral ischemic injury have also changed in the tissues ~ff hypcrlipidemia rat models, and have a certain effect on the neurons. After hyperlipidemia complicated with cerebral ischemia, whether these factors play a synergistic effect deserves a further investigation; there should be unified, specification standards in establishing hyperlipemia and cerebral ischemia models.