关键词: 血管生成抑制剂, 明胶酶B, 梗塞,大脑中动脉, 糖尿病, 大鼠,Wistar, 大鼠,GK

Abstract: To explore the pathophysiological mechanism of acute cerebral ischemia complicated with chronic diabetes by observing expressions of angiostatin protein in cerebral ischemic tissues at different ischemiareperfusion (I/R) time points. MethodsDiabetes groups［ GotoKakizaki (GK)］ and control groups(Wistar rats )were randomly subdivided into 3 groups: the shamoperation group, the cerebral ischemic groups(CI) and the cerebral ischemic complicated with diabetes groups(DM+CI). Models of focal cerebral ischemiareperfusion were established by the Longa′s technique. Western blotting and SDSPAGE zymography were used to estimated the protein expressions of angiostatin and activity of MMP9 at different I/R time points (3?h, 24?h, 3?d、7?d). ResultsExpressions of angiostatin and activity of MMP9 in ischemic brain tissues started to increase at 3?h after reperfusion, reached peaks at 24?h and then gradually decreased， but still kept at a level above the basal level at 3?d. There was a significant increase of angiostatin expression in the DM+CI group compared with that in the CI groups at 24?h(P＜0.05). Activity of MMP9 was more significantly increased in the DM+CI group than in the CI group at all I/R time points (P＜0.01). There was a linear correlation between angiostatin expressions and MMP9 activity in the DM+CI and CI groups. ConclusionIncrease of MMP9 activity contributes to the upregulation of angiostatin and it may participate in the pathology of reperfusion of diabetic infarct brains.

Key words: Angiogenesis inhibitors, Gelatinase B, Infarction,middle cerebral artery, Diabetes mellitus, Rats,Wistar, Rats,GK