AI Article Synopsis
- Several studies have indicated that cyclooxygenase-2 plays a role in the delayed progression of ischemic brain damage.
- This research focused on the effects of the selective cyclooxygenase-2 inhibitor DFU on neuronal damage in gerbils after a 5-minute episode of temporary forebrain ischemia.
- DFU treatment, even when given 12 hours after the ischemic event, significantly reduced neuronal damage in the hippocampus, suggesting that cyclooxygenase-2 inhibitors could be an effective treatment for ischemic brain injuries.
Article 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.
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| http://dx.doi.org/10.1016/s0006-8993(01)03358-3 | DOI Listing |
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