摘要
目的应用可逆性大鼠颈动脉重度狭窄合并脑梗死模型,探讨颈动脉狭窄合并脑梗死血管再通后脑组织基质金属蛋白酶-9(matrix metalloproteinase-9, MMP-9)表达的动态变化。方法采用针控线拴法和自体血栓制作可逆性大鼠颈动脉狭窄合并脑梗死模型,免疫组织化学染色及半定量脑内MMP-9的变化。结果颈动脉重度狭窄合并脑梗死无再通组梗死侧脑组织MMP-9表达增加(P<0.05), 1d开始明显增高,以后逐渐下降;5d出现第2个高峰。1d、2d、3d、5d、7d颈动脉狭窄合并脑梗死无再通组梗死侧MMP-9表达均高于非梗死侧(P<0.05);14d时颈动脉狭窄合并脑梗死无再通组梗死侧MMP-9表达与非梗死侧相比无统计学差异(P>0.05)。颈动脉重度狭窄合并脑梗死再通组MMP-9表达1d开始升高;5d达高峰;7d和14d逐渐降低。与无再通组相比各时间点MMP-9的表达均有降低趋势,第1天时降低较明显(P<0.05)。结论大鼠颈动脉重度狭窄合并脑梗死无再通组和再通组梗死侧MMP-9表达均高于非梗死侧,且MMP-9的表达与血管再通有关。
Objective To investigate the expression of matrix metalloproteinase-9 in rats following carotid artery severe stenosis complicating multiple cerebral embolism.Methods In rats,severe stenosis of the common carotid artery (CCA) was induced by ligation of common carotid artery using a needle to control the degree of stenosis,and multiple cerebral emboli were induced by injecting the autogeneic embolus through the external carotid artery.The expression of MMP-9 was then determined by immunohistochemistry assay.Results In non-recanalized CCA stenosis,level of MMP-9 expression in ischemic hemisphere was significantly higher ( P 〈0.05) than that in non-ischemic hemisphere starting from 1d,second peak on 5d,declined on 7d that was obviously above the level of contralateral side.In recanalized CCA stenosis,MMP-9 expression in ischemic hemisphere were significantly higher ( P 〈0.05) than that in non-ischemic hemisphere,which increased on 1d,peaked on 5d,and then decreased on 7d.Compared with non-recanalized CCA stenosis,the expression of MMP-9 increased markedly in recanalization group on 1d.Conclusion MMP-9 expression was induced after carotid artery severe stenosis complicating multiple embolism and recanalization.The expression of MMP-9 might be related to the time of recanalization.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2009年第2期132-135,共4页
Journal of Apoplexy and Nervous Diseases
基金
国家自然科学基金资助项目(No.30770743)
首都医学发展科研基金项目(2005-2050)
关键词
颈动脉狭窄
脑梗死
基质金属蛋白酶-9
大鼠
Carotid stenosis
Cerebral infarction
Matrix metalloproteinase-9
Rats