Expressions of the pERK1/2 and the cFos Proteins at an Early Stage of Transient Global Ischemia-reperfusion Injury in the Hippocampus of Rats
Journal of the Korean Society of Emergency Medicine
;
: 475-486, 2004.
Article
in Korean
| WPRIM
| ID: wpr-104408
ABSTRACT
PURPOSE:
This study was to evaluate temporal changes in the expressions of the phosphorylated extracellular-regulated kinase1/2 (pERK1/2), the phosphorylated MAPK/ERK kinase1/2 (pMEK1/2) and the cFos proteins in the hippocampus of rats following transient global ischemia.METHODS:
Transient global ischemia was induced in the forebrains of Sprague-Dawley rats by using a 4-vessel occlusion for 20 min under anesthetic condition. Hematoxyline-eosin staining showed typical microscopic findings that represented neuronal cell death in hippocampal CA1 regions 5 days after transient global ischemia. Four-vessel occlusion-reperfusion produced ischemic injury in major forebrain structures, such as the striatum, the cortex and the hippocampus, in the finding of triphenyltetrazolium chloride (TTC) staining.RESULTS:
A high density of pERK1/2 immunoreactivity existed in the pyramidal-cell layers of the CA2-3 regions and in the granular-cell layers of the dentate gyrus 5 min after ischemia. Following ischemia, expression of the pMEK1/2 protein showed temporal changes similar to that of the pERK1/2 protein. A significant expression of the cFos protein was noted in the pyramidal-cell layers of the CA2-3 regions and in the granular-cell layers of the dentate gyrus 2 hours after global ischemia.CONCLUSION:
Intracellular signaling cascades of the ERK or the cFos protein take part in early cellular events in the hippocampus of rats in response to ischemic insult.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Reperfusion Injury
/
Prosencephalon
/
Cell Death
/
Rats, Sprague-Dawley
/
Dentate Gyrus
/
CA1 Region, Hippocampal
/
Hippocampus
/
Ischemia
/
Neurons
Limits:
Animals
Language:
Korean
Journal:
Journal of the Korean Society of Emergency Medicine
Year:
2004
Type:
Article
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