일과성 전뇌허혈 후 뇌조직내 Polyamine 함량 변동과 신경세포 손상에 대한 Ibuprofen의 효과
- Author(s)
- 이승환; 이성룡; 임정근; 이형; 이상도; Seung-Hwan Lee; Seong-Ryong Lee; Jeong-Geun Lim; Hyung Lee; Sang-Doe Yi
- Keimyung Author(s)
- Lim, Jeong Geun; Lee, Hyung; Yi, Sang Do; Lee, Seong Ryong
- Department
- Dept. of Neurology (신경과학)
Dept. of Pharmacology (약리학)
- Journal Title
- 대한신경과학회지
- Issued Date
- 2002
- Volume
- 20
- Issue
- 3
- Abstract
- Background : In brain ischemia, increased arachidonic acid metabolism can play important roles in neuronal damage. 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 damage 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 immediately 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 global ischemia and may have putative neuroprotective effect against neuronal damage induced by global ischemia.
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