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Methyleugenol reduces cerebral ischemic injury by suppression of oxidative injury and inflammation

Authors
Choi, Yo KeumCho, Geum-SilHwang, SunyoungKim, Byung WooLim, Ji H.Lee, Jae-ChulKim, Hyoung ChunKim, Won-KiKim, Yeong Sik
Issue Date
8월-2010
Publisher
TAYLOR & FRANCIS LTD
Keywords
Methyleugenol; ischemic injury; OGD; ROS; NO
Citation
FREE RADICAL RESEARCH, v.44, no.8, pp.925 - 935
Indexed
SCIE
SCOPUS
Journal Title
FREE RADICAL RESEARCH
Volume
44
Number
8
Start Page
925
End Page
935
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/116017
DOI
10.3109/10715762.2010.490837
ISSN
1071-5762
Abstract
The present study tested the cytoprotective effect of methyleugenol in an in vivo ischemia model (i.e. middle cerebral artery occlusion (MCAO) for 1.5 h and subsequent reperfusion for 24 h) and further investigated its mechanism of action in in vitro cerebral ischemic models. When applied shortly after rcperfusion, methyleugenol largely reduced cerebral ischemic injury. Methyleugenol decreased the caspase-3 activation and death of cultured cerebral cortical neurons caused by oxygen-glucose deprivation (OGD) for 1 h and subsequent re-oxygenation for 24 h. Methyleugenol markedly reduced superoxide generation in the ischemic brain and decreased the intracellular oxidative stress caused by OGD/re-oxygenation. It was found that methyleugenol elevated the activities of superoxide dismutase and catalase. Further, methyleugenol inhibited the production of nitric oxide and decreased the protein expression of inducible nitric oxide synthase. Methyleugenol down-regulated the production of pro-inflammatory cytokines in the ischemic brain as well as in immunostimulated mixed glial cells. The results indicate that methyleugenol could be useful for the treatment of ischemia/inflammation-related diseases.
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