The highly selective cyclooxygenase-2 inhibitor DFU is neuroprotective when given several hours after transient cerebral ischemia in gerbils

TL;DR

This study demonstrates that the selective COX-2 inhibitor DFU can significantly reduce neuronal damage in gerbils even when administered several hours after transient cerebral ischemia, indicating its potential as a therapeutic agent.

Contribution

It shows that delayed administration of the COX-2 inhibitor DFU provides neuroprotection after ischemic brain injury in a gerbil model.

Findings

DFU reduces hippocampal neuronal damage when given 12 hours post-ischemia.

Treatment with DFU decreases behavioral deficits associated with ischemic injury.

Selective COX-2 inhibition may be a viable therapeutic approach for stroke.

Abstract

Several studies suggest that cyclooxygenase-2 contributes to the delayed progression of ischemic brain damage. In this study we examined whether the highly selective cyclooxygenase-2 inhibitor DFU reduces neuronal damage when administered several hours after 5 min of transient forebrain ischemia in gerbils. The extent of ischemic injury was assessed behaviorally by measuring the increases in locomotor activity and by histopathological evaluation of the extent of CA1 hippocampal pyramidal cell injury 7 days after ischemia. DFU treatment (10 mg/kg, p.o.) significantly reduced hippocampal neuronal damage even if the treatment is delayed until 12 h after ischemia. These results suggest that selective cyclooxygenase-2 inhibitors may be a valuable therapeutic strategy for ischemic brain injury.