title: Methyleugenol reduces cerebral ischemic injury by suppression of oxidative injury and inflammation.
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 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.
authors.affiliation: College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
authors.forename: Yoo Keum
authors.initials: YK
authors.lastname: Choi
authors.forename: Geum-Sil
authors.initials: GS
authors.lastname: Cho
authors.forename: Sunyoung
authors.initials: S
authors.lastname: Hwang
authors.forename: Byung Woo
authors.initials: BW
authors.lastname: Kim
authors.forename: Ji H
authors.initials: JH
authors.lastname: Lim
authors.forename: Jae-Chul
authors.initials: JC
authors.lastname: Lee
authors.forename: Hyoung Chun
authors.initials: HC
authors.lastname: Kim
authors.forename: Won-Ki
authors.initials: WK
authors.lastname: Kim
authors.forename: Yeong Sik
authors.initials: YS
authors.lastname: Kim
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005054:Eugenol / Q000031:analogs & derivatives* / Q000494:pharmacology; D005609:Free Radicals / Q000032:analysis; D005947:Glucose / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy* / Q000276:immunology; D008297:Male; D009474:Neurons / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects* / Q000276:immunology; D010100:Oxygen / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013481:Superoxides / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D005609:Free Radicals; D013481:Superoxides; C005223:methyleugenol; D005054:Eugenol; D005947:Glucose; D010100:Oxygen