脑缺血合并高脂血症模型大鼠脑组织的病理改变

Pathological changes of brain tissue in a rat model with coexistence of hyperlipidemia and cerebral ischemia

背景:大多数脑缺血是在高血压、高脂血症、糖尿病等基础病变条件下发生的。因此,构建高脂血症复合脑缺血大鼠模型,研究基础性病变对脑缺血的影响具有重要意义。目的:观察高脂血症复合脑缺血大鼠模型脑组织病理学改变,及其高脂血症病理因素对脑缺血的影响。方法:实验以高脂饲料喂养大鼠制备高脂血症大鼠模型,然后线栓法制备局灶性脑缺血大鼠模型,建模成功后 3,7 d,采用 TTC 染色的方法,观察各组大鼠脑组织缺血部位体积,苏木精-伊红染色观察各组大鼠脑组织缺血边缘区组织病理学改变,透射电镜观察各组大鼠脑组织缺血边缘区细胞超微结构改变。结果与结论:TTC 染色结果显示高脂+脑缺血 7 d 组大鼠的脑缺血部位体积明显减小。苏木精-伊红染色结果显示所有脑缺血模型都呈典型的缺血性改变,脑缺血 7 d 的小胶质细胞数量比 3 d 的明显减少,高脂+脑缺血7d 相对于 3 d 的变化更明显。超微结构显示所有脑缺血模型的神经元和胶质细胞核膜皱缩,线粒体嵴基本完全消失,内皮细胞线粒体减少,神经突触的突触小泡大部分溶解,缺血 7 d,尤其是高脂+脑缺血 7 d 的上述损伤减轻,神经元变性、坏死减少,线粒体损伤恢复,线粒体嵴也明显增多,神经突触的突触小泡明显恢复。说明高脂血症促进了脑缺血损伤的恢复,其原因可能是高脂血症因素激活了体内某种保护机制。

BACKGROUND： Cerebral ischemia often occurs in underlying pathological conditions, such as hypertension, hyperlipidemia and diabetes. Therefore, it is of great significance to construct a cerebral ischemia rat model with hyperlipidemia and to study the effect of basic pathological changes on the cerebral ischemia. OBJECTIVE： To observe the brain tissue pathological changes of rat models with coexistence of hyperlipidemia and cerebral ischemia, and the effect of hyperlipidmia on cerebral ischemia. METHODS： The rats were fed with high-fat diet to establish the hyperlipidmia models, and then focal cerebral ischemia models were prepared with suture method. At 3 and 7 days after modeling, the 2,3,5- triphenyltetrazolium chloride staining was used to observe the volume of brain tissue ischemia, and hematoxylin-eosin staining was performed to observe pathological change of the margin of the brain tissue ischemia zone. RESULTS AND CONCLUSION： 2,3,5-Triphenyltetrazolium chloride staining staining results showed that the volume of cerebral ischemia was significantly reduced in the hyperlipidemia＋cerebral ischemia 7 day group. Hematoxylin-eosin staining results showed there was typical ischemic changes in all the cerebral ischemia models, and the number of microglial cells after cerebral ischemia for 7 days was significantly smaller than that after cerebral ischemia for 3 days, and the changes were more obvious in the hyperlipidemia＋7-day cerebral ischemia group when compared with the hypedipidemia^3-day cerebral ischemia group. Ultrastructure showed there were neuronal and glial nuclear membrane shrinkage in all the cerebral ischemia models, mitochondria cristae was disappeared completely, endothelial cell mitochondria was decreased, most of the synaptic vesicles of nerve synapse were dissolved; the damages above were improved after ischemia for 7 days, especially hyperlipidemia＋cerebral ischemia for 7 days, the neuronal degeneration and necrosis were reduced, the mitochondrial damage was repaired, the number of mitochondrial cristae was increased significantly, and the synaptic vesicles of nerve synapse were recovered significantly. The results indicate that hyperlipidemia can promote the recovery of cerebral ischemic injury,pro babl=y becaus=e !he hyper!!p_ide =mia= fac!o=rscan= ac!iv=ate=th=e= =pro te=c=ti=o=n=mechanis=m=. ,, I