Tenoxicam Exerts a Neuroprotective Action after Cerebral Ischemia in Rats |
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Authors: | Rita I M Galvão João P L Diógenes Graziela C L Maia Emídio A S Filho Silvânia M M Vasconcelos Dalgimar B de Menezes Geanne M A Cunha Glauce S B Viana |
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Institution: | (1) Department of Physiology and Pharmacology, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil;(2) Department of Pathology and Legal Medicine, Faculty of Medicine, Federal University of Ceará, Fortaleza, Brazil;(3) Departamento de Fisiologia e Farmacologia, Universidade Federal do Ceará, Rua Coronel Nunes de Melo, 1127, Fortaleza, Brazil, CEP 60430-270 |
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Abstract: | In this study we investigated the effects of Tenoxicam, a type 2 cyclooxygenase (COX-2) inhibitor, on brain damage induced by ischemia-reperfusion. Male Wistar rats (18-month old average) were anesthetized and submitted to ischemia occlusion of both common carotid arteries (BCAO) for 45 min. After 24 h of reperfusion, rats were decapitated and hippocampi removed for further assays. Animals were divided into sham-operated, ischemia, ischemia + Tenoxicam 2.5 mg/kg, and ischemia + Tenoxicam 10 mg/kg groups. Tenoxicam was administered intraperitoneally immediately after BCAO. Histological analyses show that ischemia produced significant striatal as well as hippocampal lesions which were reversed by the Tenoxicam treatment. Tenoxicam also significantly reduced, to control levels, the increased myeloperoxidase activity in hippocampus homogenates observed after ischemia. However, nitrite concentrations showed only a tendency to decrease in the ischemia + Tenoxicam groups, as compared to that of ischemia alone. On the other hand, hippocampal glutamate and aspartate levels were not altered by Tenoxicam. In conclusion, we showed that ischemia is certainly related to inflammation and to increased free radical production, and selective COX-2 inhibitors might be neuroprotective agents of potential benefit in the treatment of cerebral brain ischemia. |
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Keywords: | Brain ischemia cyclooxigenase inhibitors free radicals inflammation |
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