Effect of Ibuprofen on the Changes of Polyamine Level and Neuronal Cell Damage after Transient Global Ischemia in Gerbil.
Seung Hwan Lee, Seong‐Ryong Lee, Jeong-Geun Lim, Hyung Lee, Sang-Doe Yi
Abstract
Seung Hwan Lee, Seong‐Ryong Lee, Jeong-Geun Lim, Hyung Lee, Sang-Doe Yi
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.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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.
Key concepts: Gerbil, Ischemia, Medicine, Hippocampal formation, Hippocampus, Neuroprotection, Anesthesia, Pharmacology