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Inhibition of the cerebral ischemic injury by ethyl pyruvate with a wide therapeutic window

Title
Inhibition of the cerebral ischemic injury by ethyl pyruvate with a wide therapeutic window
Authors
Yu Y.-M.Kim J.-B.Lee K.-W.Kim S.Y.Han P.-L.Lee J.-K.
Ewha Authors
한평림
SCOPUS Author ID
한평림scopus
Issue Date
2005
Journal Title
Stroke
ISSN
0039-2499JCR Link
Citation
Stroke vol. 36, no. 10, pp. 2238 - 2243
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Background and Purpose - Ethyl pyruvate (EP) is a pyruvate derivative that has been reported recently to prevent lethality in mice with established lethal sepsis and systemic inflammation. In this study, we examined the neuroprotective effect of EP in a rat cerebral ischemia model of middle cerebral artery occlusion (MCAO). Methods - Male Sprague-Dawley rats were subjected to 1 hour of MCAO, and EP was administered at various time points before or after MCAO. The changes in the brain infarction, neurological deficits, microglia activation, and proinflammatory cytokine expression were evaluated. BV2 microglial cells were also used to access the anti-inflammatory effect of EP. Results - The administration of EP intraperitoneally at 30 minutes before or at 4 or 12 hours after MCAO reduced the infarct volume to 10.3±3.4% (n=6; P<0.05), 21.5±2.7% (n=6; P<0.05), and 44.3±4.0% (n=6; P<0.05), respectively, of that of the control group. The significant reduction in infarct volume was accompanied by the suppression of the clinical manifestations associated with cerebral ischemia, including motor impairment and neurological deficits, microglial activation, and proinflammatory cytokine expression. The neuroprotective effect of EP was yet evident when it was administered as late as 24 hours after MCAO/reperfusion (76.5±4.70%; n=6; P<0.05). EP suppressed lipopolysaccharide induced activation of BV2 cells, as was evidenced by a reduction in NO release and the accompanying induction of proinflammatory cytokines. Conclusions - These results suggest that EP affords the strong protection of the delayed cerebral ischemic injury with a wide therapeutic window. © 2005 American Heart Association, Inc.
DOI
10.1161/01.STR.0000181779.83472.35
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일반대학원 > 뇌·인지과학과 > Journal papers
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