摘要
目的研究降纤酶对实验性脑梗死灶周围微血管的作用。方法用线栓法将易卒中型肾血管性高血压大鼠(stroke-pronerenovascularhypertensiverats,RHRSP)复制成一侧大脑中动脉闭塞(MCAO)模型,静脉注射降纤酶,对照组注射生理盐水,分别于缺血3、6、24h进行功能评分并处死大鼠,TTC染色计算脑梗死范围,HE染色观察梗死边缘区的病理形态,同时免疫组织化学检测尿激酶型纤溶酶原激活剂(urokinasetypeplasminogenactivator,uPA)和纤溶酶原激活剂抑制物1(plasminogenactivatorinhibitor1,PAI1)蛋白的表达。结果降纤酶能改善MCAO后神经功能评分,减少梗死灶体积,梗死灶边缘微血管损害减轻,血管内皮uPA蛋白表达减少及PAI1蛋白表达增加。结论降纤酶可能是通过抑制微血管内皮细胞uPA蛋白表达和增加PAI1蛋白表达而减轻脑梗死灶边缘微血管损害。
Objective To study the effects of defibrase on cerebromicrovessels in the marginal experimental infarction focus. Methods With stroke-prone renovascular hypertensive rats subjected to reperfusive focal middle cerebral artery occlusion （MCAO） , defibrase was injected intravenously, whereas the control groups received only normal saline, then with neurological functions scored, the rats were killed at 3, 6, 24 hours after operation. Infarction size was measured by 2,3,5-triphenyhetrazolium chloride （TTC）staining and pathological changes was observed by HE staining, and immunohistochemistry was used to detected express of urokinase-type plasminogen activator （uPA）and plasminogen activator inhibitor-1 （PAI-1）. Results In the treatment groups, neurological function scores, infarction size, cerebromicrovessel injury and PAI-1 express decreased, whereas express of uPA increased significantly, as compared with control groups, Conclusions Defibrase can relieve cerebromicrovessel injury in the marginal experimental infarction focus by inhabiting express of uPA and inducing express of PAI-1.
出处
《中国神经精神疾病杂志》
CAS
CSCD
北大核心
2006年第1期15-18,共4页
Chinese Journal of Nervous and Mental Diseases
基金
卫生部科学研究基金资助(编号:98-2-390)
关键词
降纤酶
卒中
肾血管性高血压大鼠
脑梗死
Defibrase Stroke-prone renovascular hypertensive rats Cerebral infarction
