Nimesulide limits kainate-induced oxidative damage in the rat hippocampus

TL;DR

This study demonstrates that nimesulide, a selective cyclooxygenase-2 inhibitor, reduces oxidative damage in the rat hippocampus caused by kainate, indicating a role of cyclooxygenase-2 in free radical formation.

Contribution

It provides evidence that nimesulide attenuates kainate-induced oxidative damage, highlighting its potential neuroprotective effects via cyclooxygenase-2 inhibition.

Findings

Nimesulide decreases hippocampal lipid peroxidation.

Nimesulide restores glutathione levels after kainate.

Cyclooxygenase-2 involvement in oxidative stress.

Abstract

Kainate induces a marked expression of cyclooxygenase-2 after its systemic administration. Because cyclooxygenase-2 activity is associated to the production of reactive oxygen species, we investigated the effects of nimesulide, a selective cyclooxygenase-2 inhibitor, on kainate-induced in vivo oxidative damage in the rat hippocampus. A clinically relevant dose of nimesulide (6 mg/kg, i.p.) was administered three times following kainate application (9 mg/kg, i.p.). After 24 h of kainate administration, the drastic decrease in hippocampal glutathione content and the significant increase in lipid peroxidation were attenuated in nimesulide-treated rats, suggesting that the induction of cyclooxygenase-2 is involved in kainate-mediated free radicals formation.