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作 者:王洪新[1] 梅元武[2] 陈泽峰[1] 邹永明[1] 刘家美[1]
机构地区:[1]天津市第四中心医院神经内二科,天津300140 [2]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》2007年第6期690-693,I0001,共5页Journal of Apoplexy and Nervous Diseases
基 金:天津市卫生局资助项目(07ky18)
摘 要:目的探讨超负荷血糖对脑缺血再灌注损伤大鼠MMP-2及MMP-9的表达影响。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。然后对大鼠进行脑梗死体积计算,并采用免疫组织化学方法和原位杂交方法检测超负荷血糖大鼠和正常大鼠脑缺血3h再灌注6h、12h、24h、48h、96h、7d时MMP-9及MMP-9的表达,并与假手术正常对照组比较。结果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MMP-2及MMP-9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MMP-2及MMP-9的表达异常促进了脑缺血再灌注损伤的炎症机制,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 MMP-2 and MMP-9 in the Wistar rats which suffered from focal cerebral ischemia reperfusion injury combined with diabetes and the influence under Hyperglycemia of big rats on focal cerebral ischemia reperfusion injury. Methods Hyperglycemia model was made by injection of streptozocin through abdomen in Wistar rats. At 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 infarct volume of animals were estimated. In addtion,immunohistochemistry and in situ hybridization histoehemistry were used to detect the ex- pression level of MMP-2 and MMP-9 in Wistar rats. Resuls The infarct volume was higher siginifieantly in hyperglycemic rats than which of nonhyperglycemic rats. The same things happened in the expression of MMP-2 and MMP-9 in the groups of hyperglycemic rats and nonhyperglycemic rats. Conclusion Hyperglycemia aggravates the injury of focal ischmia-reperfusion in Wistar rats and the higher expression of MMP-2 and MMP-9 may be one of the principles in aggraviated focal ischemia reperfusion injury.
关 键 词:超负荷血糖 脑缺血再灌注损伤 MMP-2 MMP-9
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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