Song Yuqiang, Zou Hongli, Wang Guofeng, Yang Hongxia, Xie Zhaohong, Bi Jianzhong
Department of Neurology, the Affiliated Hospital of Medical College, Qingdao University, Qingdao 266003, Shandong Province, China.
Qingdao Central Hospital, Qingdao 266042, Shandong Province, China.
Neural Regen Res. 2012 Jun 15;7(17):1325-30. doi: 10.3969/j.issn.1673-5374.2012.17.007.
Activity of matrix metalloproteinase-9 increases following cerebral ischemia/reperfusion, and is associated with cerebral microvascular permeability, blood-brain barrier destruction, inflammatory cell infiltration and brain edema. Matrix metalloproteinase-9 also likely participates in thrombolysis. A rat model of middle cerebral artery infarction was established by injecting autologous blood clots into the internal carotid artery. At 3 hours following model induction, urokinase was injected into the caudal vein. Decreased neurological severity score, reduced infarct volume, and increased expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 were observed in the cerebral cortex 24 hours after urokinase thrombolysis. These results suggest that urokinase can suppress damage in the acute-early stage of cerebral infarction.
脑缺血/再灌注后基质金属蛋白酶-9的活性增加，且与脑微血管通透性、血脑屏障破坏、炎性细胞浸润和脑水肿相关。基质金属蛋白酶-9也可能参与溶栓过程。通过向颈内动脉注射自体血凝块建立大鼠大脑中动脉梗死模型。在模型诱导后3小时，将尿激酶注入尾静脉。尿激酶溶栓24小时后，观察到大脑皮质神经功能严重程度评分降低、梗死体积减小，以及基质金属蛋白酶-9和金属蛋白酶组织抑制剂-1的表达增加。这些结果表明，尿激酶可在脑梗死急性早期抑制损伤。
