Delayed treatment with nimesulide reduces measures of oxidative stress following global ischemic brain injury in gerbils

Metabolism of arachidonic acid by cyclooxygenase is one of the primary sources of reactive oxygen species in the ischemic brain. Neuronal overexpression of cyclooxygenase-2 has recently been shown to contribute to neurodegeneration following ischemic injury. In the present study, we examined the pos...

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Bibliographic Details
Published in:Neuroscience research 2003-10, Vol.47 (2), p.245-253
Main Authors: Candelario-Jalil, Eduardo, Alvarez, Dalia, Merino, Nelson, León, Olga Sonia
Format: Article
Language:English
Subjects:
Animals
Brain Ischemia - drug therapy
Brain Ischemia - metabolism
Cerebral ischemia
Cyclooxygenase 2
Dose-Response Relationship, Drug
Fluoro-Jade B
Gerbillinae
Glutathione
Isoenzymes - metabolism
Lipid peroxidation
Lipid Peroxidation - drug effects
Lipid Peroxidation - physiology
Male
Neurodegeneration
Nimesulide
Oxidative stress
Oxidative Stress - drug effects
Oxidative Stress - physiology
Prostaglandin-Endoperoxide Synthases - metabolism
Sulfonamides - administration & dosage
Time Factors
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Summary:Metabolism of arachidonic acid by cyclooxygenase is one of the primary sources of reactive oxygen species in the ischemic brain. Neuronal overexpression of cyclooxygenase-2 has recently been shown to contribute to neurodegeneration following ischemic injury. In the present study, we examined the possibility that the neuroprotective effects of the cyclooxygenase-2 inhibitor nimesulide would depend upon reduction of oxidative stress following cerebral ischemia. Gerbils were subjected to 5 min of transient global cerebral ischemia followed by 48 h of reperfusion and markers of oxidative stress were measured in hippocampus of gerbils receiving vehicle or nimesulide treatment at three different clinically relevant doses (3, 6 or 12 mg/kg). Compared with vehicle, nimesulide significantly ( P
ISSN:0168-0102
1872-8111
DOI:10.1016/S0168-0102(03)00184-6