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

Brain Res. 2002 Feb 15;927(2):212-5. doi: 10.1016/s0006-8993(01)03358-3.

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.

MeSH terms

  • Animals
  • Brain Ischemia / enzymology*
  • Brain Ischemia / physiopathology
  • Brain Ischemia / prevention & control*
  • Cell Death / drug effects
  • Cyclooxygenase 2
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors / pharmacology*
  • Cyclooxygenase Inhibitors / therapeutic use
  • Furans / pharmacology*
  • Furans / therapeutic use
  • Gerbillinae
  • Hippocampus / drug effects
  • Hippocampus / pathology
  • Isoenzymes / antagonists & inhibitors*
  • Locomotion / drug effects
  • Male
  • Neuroprotective Agents / pharmacology*
  • Neuroprotective Agents / therapeutic use
  • Prostaglandin-Endoperoxide Synthases

Substances

  • 5,5-dimethyl-3-(3-fluorophenyl)-4-(4-methylsulfonyl)phenyl-2(5H)-furanone
  • Cyclooxygenase 2 Inhibitors
  • Cyclooxygenase Inhibitors
  • Furans
  • Isoenzymes
  • Neuroprotective Agents
  • Cyclooxygenase 2
  • Prostaglandin-Endoperoxide Synthases