Metalloproteinase and stroke infarct size: role for anti-inflammatory treatment?

被引:122
作者
Morancho, Anna [1 ]
Rosell, Anna [1 ]
Garcia-Bonilla, Lidia [1 ]
Montaner, Joan [1 ]
机构
[1] Univ Autonoma Barcelona, Hosp Univ Vall Hebron, Inst Recerca VHIR, Dept Neurol,Neurovasc Res Lab, Barcelona, Spain
来源
INNATE INFLAMMATION AND STROKE | 2010年 / 1207卷
关键词
stroke; biomarkers; ischemia; thrombolysis; metalloproteinases; BLOOD-BRAIN-BARRIER; FOCAL CEREBRAL-ISCHEMIA; MATRIX METALLOPROTEINASES; HEMORRHAGIC TRANSFORMATION; UP-REGULATION; NEUTROPHIL INFILTRATION; TEMPORAL PROFILE; ARTERY OCCLUSION; CELL-MIGRATION; MATRIX-METALLOPROTEINASE-9;
D O I
10.1111/j.1749-6632.2010.05734.x
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Deregulation of matrix metalloproteinases (MMPs), the largest class of human proteases, has been implicated in brain damage in both animal and human studies. Some MMPs are elevated after stroke (both in plasma and in brain tissue), and their expression is enhanced by t-PA during thrombolysis related to hemorrhagic transformation events. Although the exact cellular source of MMPs remains unknown, brain endothelium, astrocytes, neurons, and inflammatory-activated cells, such as neutrophils, may release MMP-2, MMP-3, MMP-8, MMP-9, MMP-10, and/or MMP-13. Neurovascular perturbations occurring after stroke lead to blood-brain barrier leakage, edema, hemorrhage, leukocyte infiltration, and progressive inflammatory reactions to brain injury over hours or even days after the initial stroke. Synthesized MMP inhibitors and several compounds used for stroke secondary prevention, such as anti-inflammatory drugs, might decrease MMPs and improve the acute treatment of human brain ischemia without compromising the beneficial effects of matrix plasticity during stroke recovery.
引用
收藏
页码:123 / 133
页数:11
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