中國醫藥大學機構典藏 China Medical University Repository, Taiwan:Item 310903500/1609
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 29490/55136 (53%)
造访人次 : 1508055      在线人数 : 739
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧：
  • 您可在西文检索词汇前后加上"双引号"，以获取较精准的检索结果
  • 若欲以作者姓名搜寻，建议至进阶搜寻限定作者字段，可获得较完整数据
    •  进阶搜寻
    主页 ‧ 登入 ‧ 上传 ‧ 说明 ‧ 关于CMUR ‧ 管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.cmu.edu.tw/ir/handle/310903500/1609


    题名: Protective effects of magnolol against oxidized LDL-induced apoptosis in endothelial cells
    作者: 歐秀中(Hsiu-Chung Ou);周芬碧(Chou FP);許惠恒(Sheu WH);徐士蘭(Hsu SL);李文珍(Lee WJ)*
    贡献者: 健康照護學院物理治療學系
    关键词: Endothelium；OxLDL；Magnolol；Apoptosis；Mitochondrial membrane potential；Calcium homeostasis
    日期: 2007-06
    上传时间: 2009-08-19 17:04:04 (UTC+8)
    摘要: Magnolol, a compound extracted from the Chinese medicinal herb Magnolia officinalis, has several biological effects. However, its protective effects against endothelial injury remain unclear. In this study, we examined whether magnolol prevents oxidized low density lipoprotein (oxLDL)-induced vascular endothelial apoptosis. Incubation of oxLDL with magnolol (2.5-20 microM) inhibited copper-induced oxidative modification via diene formation, thiobarbituric acid reactive substances (TBARS) assay and electrophoretic mobility assay. Apoptotic cell death as characterized by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) stain. We measured the production of reactive oxygen species (ROS) by using the fluorescent probe 2',7'-dichlorofluorescein acetoxymethyl ester (DCF-AM), and observed the activity of antioxidant enzymes. Furthermore, several apoptotic signaling pathways which showed NF-kappaB activation, increased cytosolic calcium, alteration of mitochondrial membrane potential, cytochrome c release and activation of caspase 3 were also investigated. We demonstrated that magnolol prevented the copper-induced oxidative modification of LDL. Magnolol attenuated the oxLDL-induced ROS generation and subsequent NF-kappaB activation. Furthermore, intracellular calcium accumulation and subsequent mitochondrial membrane potential collapse, cytochome c release and activation of caspase 3 caused by oxLDL were also inhibited by magnolol. Our results suggest that magnolol may have clinical implications in the prevention of atherosclerotic vascular disease through decreasing the oxLDL-induced ROS production.
    關聯: ARCHIVES OF TOXICOLOGY6(81):421~432
    显示于类别:[物理治療學系(停用)] 期刊論文

    文件中的档案:

    没有与此文件相关的档案.



    在CMUR中所有的数据项都受到原著作权保护.

    TAIR相关文章

     

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈