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

Yoo Keum Choi, Geum Sil Cho, Sunyoung Hwang, Byung Woo Kim, Ji H. Lim, Jae Chul Lee, Hyoung Chun Kim, Won Ki Kim, Yeong Sik Kim

Research output: Contribution to journalArticlepeer-review

56 Citations (Scopus)


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 reperfusion, 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.

Original languageEnglish
Pages (from-to)925-935
Number of pages11
JournalFree Radical Research
Issue number8
Publication statusPublished - 2010 Aug


  • Methyleugenol
  • NO
  • OGD
  • ROS
  • ischemic injury

ASJC Scopus subject areas

  • Biochemistry


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