文化大學機構典藏 CCUR:Item 987654321/2815
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    题名: Taxifolin ameliorates cerebral ischemia-reperfusion injury in rats through its anti-oxidative effect and modulation of NF-kappa B activation
    作者: Wang YH
    Wang WY
    Chang CC
    Liou KT
    Sung YJ
    Liao JF
    Chen CF
    Chang S
    Hou YC
    Chou YC
    Shen YC
    贡献者: 國術系
    关键词: cerebral ischemic-reperfusion
    COX-2
    ICAM-1 (CD54)
    iNOS
    Mac-1 (CD11b/CD18)
    nuclear factor kappa B (NF-kappa B)
    reactive oxygen species
    taxifolin
    日期: 2006
    上传时间: 2009-11-20 15:53:56 (UTC+8)
    摘要: Infarction in adult rat brain was induced by middle cerebral arterial occlusion (MCAO) followed by reperfusion to examine whether taxifolin could reduce cerebral ischemic reperfusion (CI/R) injury. Taxifolin administration (0.1 and 1.0 mu g/kg, i.v.) 60 min after MCAO ameliorated infarction (by 42%+/- 7% and 62%+/- 6%, respectively), which was accompanied by a dramatic reduction in malondialdehyde and nitrotyrosine adduct formation, two markers for oxidative tissue damage. Overproduction of reactive oxygen species (ROS) and nitric oxide (NO) via oxidative enzymes (e.g., COX-2 and iNOS) was responsible for this oxidative damage. Taxifolin inhibited leukocyte infiltration, and COX-2 and iNOS expressions in CI/R-injured brain. Taxifolin also prevented Mac-1 and ICAM-1 expression, two key counter-receptors involved in firm adhesion/transmigration of leukocytes to the endothelium, which partially accounted for the limited leukocyte infiltration. ROS, generated by leukocytes and microglial cells, activated nuclear factor-kappa B (NF-kappa B) that in turn signaled up-regulation of inflammatory proteins. NF-kappa B activity in CI/R was enhanced 2.5-fold over that of sham group and was inhibited by taxifolin. Production of both ROS and NO by leukocytes and microglial cells was significantly antagonized by taxifolin. These data suggest that amelioration of CI/R injury by taxifolin may be attributed to its anti-oxidative effect, which in turn modulates NF-kappa B activation that mediates CI/R injury.
    關聯: JOURNAL OF BIOMEDICAL SCIENCE Volume: 13 Issue: 1 Pages: 127-141
    显示于类别:[技擊運動暨國術學系] 期刊論文

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