Tenoxicam exerts a neuroprotective action after cerebral ischemia in rats

• Published in: Neurochemical research Vol. 30; no. 1; pp. 39 - 46
• Main Authors: Galvão, Rita I M, Diógenes, João P L, Maia, Graziela C L, Filho, Emídio A S, Vasconcelos, Silvânia M M, de Menezes, Dalgimar B, Cunha, Geanne M A, Viana, Glauce S B
• Format: Journal Article
• Language: English
• Published: United States Springer Nature B.V 01-01-2005
• Subjects: Animals; Brain - drug effects; Brain - metabolism; Brain Ischemia - drug therapy; Brain Ischemia - metabolism; Brain Ischemia - pathology; Dose-Response Relationship, Drug; Male; Neuroprotective Agents - pharmacology; Neuroprotective Agents - therapeutic use; Nitrites - metabolism; Piroxicam - analogs & derivatives; Piroxicam - pharmacology; Piroxicam - therapeutic use; Rats; Rats, Wistar
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-004-9684-5

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.