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

doi:10.3969/j.issn.2095-4344.2013.07.014

Abstract

Abstract:

BACKGROUND: Glial cells 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 metalloproteinase-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 immunohistochemical staining.
RESULTS AND CONCLUSION: The typical pathologic changes at early ischemia stage were characterized by microinfarction, mainly occurring in the cortex, basal forebrain, 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.

Key words: tissue construction, experimental modeling in tissue construction, vascular dementia, leukoaraiosis, demyelination, glial cell response, matrix metalloproteinase-9, tissue construction photographs-containing paper

CLC Number:

R318

Wang Min, Cao Bing-zhen. Glial cell responses and matrix metalloproteinase-9 expression in the brain of chronic vascular dementia rat models[J]. Chinese Journal of Tissue Engineering Research, 2013, 17(7): 1212-1219.

Figures/Tables 9

2.3 各组大鼠脑组织学观察苏木精-伊红、KB及Bodian染色：见图2-4。模型组大鼠缺血1-3 d，额颞叶皮质及海马区锥体细胞缺血水肿呈三角形，缺血7-14 d，皮质下及脑室周围出现较多梗死灶，以海马及新皮质的3，5，6层神经细胞及尾状核等纹状体区神经细胞坏死最明显。可见较多炎性细胞浸润，主要是单核吞噬细胞，海马CA1区锥体细胞及齿状回细胞减少。缺血一两个月除上述表现外，脑室周围白质疏松呈空泡样变，海马区锥体细胞严重脱失、基质疏松及微空泡形成，星形胶质细胞明显增生，白质疏松更加明显。KB染色可见髓鞘脱失，Bodian染色示轴索连续性完好。缺血三四个月，白质疏松更加明显，髓鞘脱失明显，Bodian染色未见轴索断裂，纤维性星形胶质细胞明显增多。可见部分炎性细胞围绕小静脉周围形成袖套样改变。免疫组织化学染色：见图5-7。正常组及假手术组大鼠未发现阳性小胶质细胞，未见基质金属蛋白酶9表达，在皮质及白质内可见散在星形胶质细胞。缺血1 d，皮质、基底节、内囊、胼胝体、海马、视束等处均有胞浆染色阳性的小胶质细胞；基质金属蛋白酶9表达在缺血3-7 d以海马CA1区增加明显；缺血7-14 d脑室周围白质小胶质细胞显著增多，梗死灶周围小胶质细胞增生明显。缺血1个月，小胶质细胞反应达到高峰，小胶质细胞和基质金属蛋白酶9的表达以室周白质最为显著，其次是皮质和海马；梗死中心区阿米巴状、圆状小胶质细胞高度聚集，梗死区周边见高分枝状小胶质细胞；缺血2-4个月后仍以室周白质及白质疏松处最显著，而海马区小胶质细胞活动则减少。胶质纤维酸性蛋白阳性星形胶质细胞在时间、空间分布及反应程度上与小胶质细胞反应相平行，形态上也经历了早期的纤维性星形胶质细胞，到胞体增大、肿胀，树突增粗，胞浆深染的反应性星形胶质细胞，后期则出现较多的纤维性星形胶质细胞。"

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