J Korean Neurol Assoc.
2002 May;20(3):265-272.
Effect of Ibuprofen on the Changes of Polyamine Level and Neuronal Cell Damage after Transient Global Ischemia in Gerbil
- Affiliations
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- 1Department of Neurology, School of Medicine, Keimyung University, Korea. sdlee@dsmc.or.kr
- 2Department of Pharmacology, School of Medicine, Keimyung University, Korea.
Abstract
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BACKGROUND: In brain ischemia, increased arachidonic acid metabolism can play important roles in neuronal dam-age. Ibuprofen was reported to have a protective role against neuronal damage in focal brain ischemia and reperfusion. The present study was designed to investigate whether ibuprofen can inhibit the global ischemia-induced neuronal dam-age and changes of polyamine (PA) level which is known to related to the neuronal damage, breakdown of blood brain barrier, and brain edema.
METHODS
Male Mongolian gerbils were used in this study. Transient global ischemia was induced by occlusion of bilateral common carotid arteries for 3 min with microclips. Ibuprofen was administered imme-diately after ischemia. The animals were sacrificed one day after ischemia for PA measurement and sacrificed 5 days after ischemia for histological evaluation. Histological examination was performed by counting surviving neuronal cells in one mm of CA1 area in dorsal hippocampus.
RESULTS
Cerebral cortex and hippocampal putrescine(PU) levels in vehicle-treated ischemic group significantly increased comparing to sham-operated animals and the increase of PU was attenuated by ibuprofen administration (50 mg/kg). Hippocampal spermine level decreased significantly after ischemia. Hippocampal neuronal cell damage in CA1 area was markedly observed in vehicle-treated animals compared to sham operated animals. Ibuprofen administration at the dose of 50 mg/kg significantly inhibited hippocampal CA1 neuronal damage compared to vehicle-treated animals.
CONCLUSIONS
Ibuprofen attenuates PA response following transient glob-al ischemia and may have putative neuroprotective effect against neuronal damage induced by global ischemia.
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