Polymorphonuclear neutrophils contribute to infarction and oxidative stress in the cortex but not in the striatum after ischemia–reperfusion in rats
| Autor: | Isabelle Margaill, Nicole Croci, Michel Plotkine, Virginie Beray-Berthat |
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| Rok vydání: | 2003 |
| Předmět: |
Male
medicine.medical_specialty Neutrophils Ischemia Brain damage Striatum Vinblastine medicine.disease_cause Brain Ischemia Rats Sprague-Dawley Lesion Internal medicine Basal ganglia medicine Animals Molecular Biology Peroxidase Cerebral Cortex biology business.industry Cerebral infarction General Neuroscience medicine.disease Antineoplastic Agents Phytogenic Corpus Striatum Rats Oxidative Stress Endocrinology Neutrophil Infiltration Reperfusion Injury Myeloperoxidase Anesthesia biology.protein Neurology (clinical) medicine.symptom business Oxidative stress Developmental Biology |
| Zdroj: | Brain Research. 987:32-38 |
| ISSN: | 0006-8993 |
| DOI: | 10.1016/s0006-8993(03)03224-4 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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