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Polymorphonuclear neutrophils contribute to infarction and oxidative stress in the cortex but not in the striatum after ischemia-reperfusion in rats
被引:49
作者:

Beray-Berthat, V
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机构:
Univ Paris 05, Lab Pharmacol, UPRES EA 2510, F-75006 Paris, France Univ Paris 05, Lab Pharmacol, UPRES EA 2510, F-75006 Paris, France

Croci, N
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Univ Paris 05, Lab Pharmacol, UPRES EA 2510, F-75006 Paris, France Univ Paris 05, Lab Pharmacol, UPRES EA 2510, F-75006 Paris, France

Plotkine, M
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Univ Paris 05, Lab Pharmacol, UPRES EA 2510, F-75006 Paris, France Univ Paris 05, Lab Pharmacol, UPRES EA 2510, F-75006 Paris, France

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机构:
[1] Univ Paris 05, Lab Pharmacol, UPRES EA 2510, F-75006 Paris, France
关键词:
cerebral ischemia;
neutrophil infiltration;
myeloperoxidase;
vinblastine;
neutropenia;
glutathione;
D O I:
10.1016/S0006-8993(03)03224-4
中图分类号:
Q189 [神经科学];
学科分类号:
071006 ;
摘要:
The present work examined whether polymorphonuclear neutrophil (PMN) infiltration contributes to cortical and striatal brain damage and oxidative stress in a model of transient focal cerebral ischemia. A 2-h occlusion of the left middle cerebral artery and ipsilateral common carotid artery was performed in rats. Administration of the neutropenic agent vinblastine (0.5 mg/kg, i.v.) resulted in a profound decrease in circulating PMNs which was associated with a 80% decrease in myeloperoxidase activity, a marker of PMN infiltration, in both the cortex and the striatum. In the cortex, vinblastine-treated animals exhibited a 44% decrease in the infarct volume and also reduced the oxidative stress (evaluated by the decrease in glutathione concentrations). By contrast, in the striatum, neutropenia modified neither the lesion size nor the oxidative stress. These results indicate that PMN contribution to postischemic injury and oxidative stress is dependent on the brain structure. (C) 2003 Elsevier B.V. All rights reserved.
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页码:32 / 38
页数:7
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