慢性血管性痴呆模型大鼠脑胶质细胞反应及基质金属蛋白酶9的表达

背景：胶质细胞及炎性细胞因子参与了血管性痴呆慢性脑缺血的炎性反应过程。目的：观察慢性脑缺血致血管性痴呆大鼠的脑组织中胶质细胞反应及基质金属蛋白酶9的表达。方法：雄性Wistar大鼠随机分为正常组、假手术组和模型组3组。模型组通过永久性结扎大鼠的双侧颈总动脉导致慢性脑缺血建立动物模型，假手术组除不结扎双侧颈总动脉外，其余处理与模型组相同。各组大鼠行Morris水迷宫试验检测大鼠的学习记忆能力。采用病理染色、免疫组化的方法，观察大鼠在缺血后不同时间点脑组织中胶质细胞及基质金属蛋白酶9的病理改变。结果与结论：缺血早期的病理变化主要发生在皮质、基底前脑、海马、胼胝体、颞叶皮质及视束，部分出现小的梗死灶。缺血1个月后，白质髓鞘脱失、间质疏松呈空泡样改变逐渐明显，神经轴索连续性完好。小胶质细胞、星形胶质细胞及基质金属蛋白酶9的表达在缺血早期以皮质及海马为主，缺血后期以室周白质及白质疏松处更为明显，海马区表达则减少。

Glial cell responses and matrix metalloproteinase-9 expression in the brain of chronic vascular dementia rat models

BACKGROUND： Glial ceils and inflammatory cytokines are involved in the chronic inflammatory reaction process of cerebral ischemia. OBJECTIVE： To explore the glial cells response and the expression of matrix metalloproteinase-9 in the brain tissue of chronic vascular dementia Wistar rats. METHODS： Male Wistar rats were randomly divided into a normal group, a sham-operation group and a model group. Vascular dementia models were established in the model group by permanently occluding the bilateral common carotid arteries. The sham operation had no bilateral common carotid artery occlusion. The ability of learning and memory was tested by using the Morris water maze. The pathological changes of glial cells and matrix metalioproteinase-9 in rat＇s brain tissue were dynamically observed at 1, 3, 7, 14 days, 1, 2, 3, and 4 months after cerebral ischemia by using histopathologic staining and immun0histochemical staining.RESULTS AND CONCLUSION： The typical pathologic changes at early ischemia stage were characterized by microinfarction, mainly occurring in the cortex, basal forebrein, hippocampus, corpus callosum, temporal cortex and optic tract. After 1 month of bilateral common carotid artery occlusion, demyelination, stroma rarefaction and vacuolations were observed in the white matter, while axons were well preserved. Reactive microgliosis, astrogliosis and expressions of matrix metalloproteinase-9 mainly occurred in the cortex and hippocampus at early ischemia stage, while in the periventricular white matter and leukoaraiosis regions at late ischemia stage, but a reduction in the hippocampus.