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Effects of the cyclooxygenase-2 inhibitor nimesulide on cerebral infarction and neurological deficits induced by permanent middle cerebral artery occlusion in the rat
Candelario-Jalil, Eduardo; Mhadu, Noël H; González-Falcón, Armando; García-Cabrera, Michel; Muñoz, Eduardo; León, Olga Sonia; Fiebich, Bernd L.
Affiliation
  • Candelario-Jalil, Eduardo; Department of Pharmacology. University of Havana. Havana. Cuba
  • Mhadu, Noël H; Department of Pharmacology. University of Havana. Havana. Cuba
  • González-Falcón, Armando; Department of Pharmacology. University of Havana. Havana. Cuba
  • García-Cabrera, Michel; Department of Pharmacology. University of Havana. Havana. Cuba
  • Muñoz, Eduardo; Departamento de Biología Celular. Fisiología e Inmunología. Universidad de Córdoba. Córdoba. Spain
  • León, Olga Sonia; Department of Pharmacology. University of Havana. Havana. Cuba
  • Fiebich, Bernd L; VivaCell Biotechnology GmbH. University of Freiburg Medical School. Denzlingen. Germany
J Neuroinflammation ; 2(1)Jan. 2005. tab
Article in English | CUMED | ID: cum-39989
Responsible library: CU1.1
ABSTRACT

Background:

Previous studies suggest that the cyclooxygenase-2 (COX-2) inhibitor nimesulide has a remarkable protective effect against different types of brain injury including ischemia. Since there are no reports on the effects of nimesulide on permanent ischemic stroke and because most cases of human stroke are caused by permanent occlusion of cerebral arteries, the present study was conducted to assess the neuroprotective efficacy of nimesulide on the cerebral infarction and neurological deficits induced by permanent middle cerebral artery occlusion (pMCAO) in the rat. MethodsIschemia was induced by permanent occlusion of the middle cerebral artery in rats, via surgical insertion of a nylon filament into the internal carotid artery. Infarct volumes (cortical, subcortical and total) and functional recovery, assessed by neurological score evaluation and rotarod performance test, were performed 24 h after pMCAO. In initial experiments, different doses of nimesulide (3, 6 and 12 mg/kg; i.p) or vehicle were administered 30 min before pMCAO and again at 6, 12 and 18 h after stroke. In later experiments we investigated the therapeutic time window of protection of nimesulide by delaying its first administration 0.5–4 h after the ischemic insult. ResultsRepeated treatments with nimesulide dose-dependently reduced cortical, subcortical and total infarct volumes as well as the neurological deficits and motor impairment resulting from permanent ischemic stroke, but only the administration of the highest dose (12 mg/kg) was able to significantly (P < 0.01) diminish infarct volume. The lower doses failed to significantly reduce infarction but showed a beneficial effect on neurological function. Nimesulide (12 mg/kg) not only reduced infarct volume but also enhanced functional recovery when the first treatment was given up to 2 h after stroke(AU)
RESUMEN
Estudios previos sugieren que la ciclooxigenasa-2 (COX-2) tiene un inhibidor de nimesulida notable efecto protector contra diferentes tipos de lesiones cerebrales incluyendo isquemia. Dado que no existen informes sobre los efectos de la nimesulida sobre el ictus isquémico y permanente, porque la mayoría de los casos de los accidentes cerebrovasculares son causados por la oclusión permanente de arterias cerebrales, el presente estudio se llevó a cabo para evaluar la eficacia de nimesulida neuroprotectores en el infarto cerebral y déficit neurológico inducido permanente por la oclusión de arteria cerebral media (pMCAO) en la rata.

Métodos:

Isquemia fue inducida por la oclusión permanente de la arteria cerebral media en ratas, a través de la inserción quirúrgica de un filamento de nylon en la arteria carótida interna. Infarto volúmenes (corticales, subcorticales y total) y la recuperación funcional, evaluado por la puntuación de evaluación neurológica y rotarod prueba de eficacia, se han realizado 24 horas después de pMCAO. En los experimentos iniciales, diferentes dosis de nimesulida (3, 6 y 12 mg / kg, ip) o vehículo fueron administrados 30 min antes de pMCAO y de nuevo a los 6, 12 y 18 h después del accidente cerebrovascular. Más tarde en los experimentos terapéuticos que investigó la ventana de tiempo de protección de la nimesulida por retrasar su primera administración 0.5-4 horas después de la injuria isquémica.

Resultados:

Tratamientos repetidos con nimesulida dosis-dependiente reducido corticales, subcorticales y el total de los volúmenes de infarto, así como el déficit neurológico y alteraciones motoras permanentes derivadas de accidente
Subject(s)

Full text: Available Collection: National databases / Cuba Database: CUMED Main subject: Infarction, Middle Cerebral Artery / Cyclooxygenase 2 Inhibitors Language: English Journal: J Neuroinflammation Year: 2005 Document type: Article Institution/Affiliation country: Departamento de Biología Celular/Spain / Department of Pharmacology/Cuba / VivaCell Biotechnology GmbH/Germany

Full text: Available Collection: National databases / Cuba Database: CUMED Main subject: Infarction, Middle Cerebral Artery / Cyclooxygenase 2 Inhibitors Language: English Journal: J Neuroinflammation Year: 2005 Document type: Article Institution/Affiliation country: Departamento de Biología Celular/Spain / Department of Pharmacology/Cuba / VivaCell Biotechnology GmbH/Germany
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