超负荷血糖对大鼠脑缺血再灌注损伤的影响及其uPA、uPAR的表达  

The influence of hyperglycemia on focal cerebral ischemic reperfusion injury of big rats and the expression of uPA,uPAR

作　　者：王洪新[1] 梅元武[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院神经科,湖北武汉430022

出　　处：《中风与神经疾病杂志》2005年第2期145-148,共4页Journal of Apoplexy and Nervous Diseases

摘　　要：目的　观察超负荷血糖对大鼠脑缺血再灌注损伤的影响,并探讨其机制。方法　用Wistar大鼠腹腔内注射链脲佐菌素,建立超负荷糖尿病大鼠模型,之后做大脑中动脉脑缺血再灌注模型。然后对大鼠进行神经功能评分,进行脑梗死体积计算并且采用免疫组织化学和RT- PCR的方法检测超负荷血糖大鼠和正常大鼠脑缺血3h再灌注2 4 h u PA(尿激酶型纤溶酶原激活物)、u PAR(尿激酶型纤溶酶原激活物受体)的表达,并与假手术正常对照组比较。结果　超负荷血糖组大鼠神经功能评分明显高于非超负荷血糖组,超负荷血糖组梗死面积明显大于非超负荷血糖组;同时,前者u PA、u PAR的表达明显高于后者。结论　超负荷血糖加重了大鼠脑缺血再灌注损伤,超负荷血糖诱发的u PA、u PAR的表达增高可能是其加重脑缺血再灌注损伤的机制之一。Objective To study the expression of uPA、uPAR in the big wistar rats which suffered from focal cerebral ischemia reperfusion injury combined with diabetes and the influence under Hyperglycemia of big rats on focal cerebral ischemic reperfusion injury.Methods Hyperglycemia model was made by injection of streptozocin through abdomen in Wistar rats;At the the same time,focal cerebral ischemia injury was made by occluding the middle cerebral artery with lynon line in streptocin-induced hyperglycemic rats and then the scores of neurological deficit as well as infarct volume were estimated.Inaddition,immunohistochemistry and RT-PCR were used to detect the expression level of uPA、uPAR in wistar rats.Resuls The infarct volume and the scores of neurological deficit was higher siginificantly in hyperglycemic rats than which of nonhyperglycemic rats.the same things happened in the expression of uPA、uPAR in the groups of hyperglycemic rats and nonhyperglycemic rats.Conclusion Hyperglycemia aggreviates the injury of focal ischmia-reperfusion in Wistar rats and the higher expression of uPA、uPAR may be one of the principles in aggraviated focal ischemia reperfusion injury.

关 键 词：脑缺血再灌注损伤 超负荷血糖 UPAR 尿激酶型纤溶酶原激活物受体 Wistar大鼠 脑缺血再灌注模型 神经功能评分 RT-PCR 免疫组织化学 链脲佐菌素 腹腔内注射 大脑中动脉 大鼠脑缺血 正常对照组 大鼠模型 体积计算 梗死面积 

分 类 号：R743.3[医药卫生—神经病学与精神病学] R743.302[医药卫生—临床医学]