基质金属蛋白酶2与脑梗死

血清基质金属蛋白酶2(MMP-2)可通过降解基底膜,破坏血脑屏障,形成血管源性脑水肿,激活炎性细胞因子,介导炎性反应,引起炎性细胞浸润,通过直接导致持续性的细胞凋亡等机制参与脑梗死后缺血/再灌注脑损伤;MMP-2不仅参与动脉粥样硬化斑块的形成,而且其水平增高可导致动脉粥样硬化斑块不稳定并形成血栓;血清MMP-2可能对判断脑梗死的病情程度、病损范围和预后具有预测作用,因此MMP-2与脑梗死的发生、发展密切相关。抑制MMP-2的活性可能用于脑梗死的预防和治疗。

Matrix Metalloproteinase-2 and Cerebral Infarction

matrix metalloproteinase-2 （MMP-2）is involved in isehemia/reperfusion injured by disrupting basement membrane, damaging the blood-brain barrier, formatting vasogenic brain edema, activating inflammatory eytokines, mediating inflammatory response, causing inflammatory cell infiltration, directly leading to ongoing cell apoptosis. MMP-2 involves in formation of atheroscleretie plaque and the high level can induce rupture of atherosclerotie plaque. The serum levels of MMpo2 can help to predict the degree of clinical condition, sizes of the lesions and prognosis of cerebral infarction patients. MMP- 2 may be associated with occurrence and development of cerebral infarction. Inhibiting the activity of MMP-2 may be useful in the prevention and treatment of cerebral infarction.