ASIA unversity:Item 310904400/16325
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 90120/105278 (86%)
造访人次 : 8950292      在线人数 : 70
RC Version 6.0 © 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


    题名: Emodin Has Cytotoxic and Protective Effects in Rat C6 Glioma Cells: Roles of Mdr1a and Nuclear Factor kB in Cell Survival
    作者: Tzu-Ching Kuo;郭子靖;Jai-Sing Yang;楊家欣;Meng-Wei Lin;林孟葳;Shu-Chun Hsu;徐素琴;Jen-Jyh Lin;Hui-Ju Lin;林慧茹;Te-Chun Hsia;Ching-Lung Liao;廖慶隆;Mei-Due Yang;楊美都;Ming-Jen Fan;范宗宸;W. G. Wood;Jing-Gung Chung;鍾景光
    贡献者: 生物科技學系
    日期: 2009-06
    上传时间: 2012-11-23 17:11:30 (UTC+8)
    摘要: 1,3,8-Trihydroxy-6-methylanthaquinone (emodin) is recognized as an antiproliferative compound. In the present study, however, we show that emodin has both toxic and survival effects in glioma cells and that the survival effects involve Mdr1a. Emodin inhibited the proliferation and induced apoptosis of C6 cells in a 12-h treatment, but C6 cells survived a 72-h drug treatment, indicating resistance to emodin. Emodin-induced apoptosis was reduced by inhibition of the expression and activation of apoptosis-associated proteins including p53, Bax, Bcl-2, Fas, and caspase-3. C6 cells could express antioxidant proteins (superoxide dismutase and catalase) to decrease reactive oxygen species-induced cytotoxicity of emodin and overexpress multidrug resistance genes (Mdr1a, MRP2, MRP3, and MRP6) to decrease the intracellular accumulation of emodin. Electrophoretic mobility shift analysis showed that emodin decreased nuclear factor κB (NF-κB) expression in 24 h of treatment, but in 48 h, emodin increased NF-κB activity. A confocal microscope showed that emodin induced NF-κB translocation from cytoplasm to nuclei. C6 cells would activate the mitogen-activated protein kinase survival pathway and express the DNA repair gene (MGMT) and associated proteins (PARP and XRCC1) to recover the cell activity. C6 cells also expressed GRP78 to decrease emodin-induced endoplasmic reticulum (ER) stress that would cause apoptosis in C6 cells, and GRP78 inhibited the expression of GADD153 to enhance the expression of Bcl-2 that could balance the ER- and mitochondria-induced apoptosis of C6 cells.
    關聯: The Journal of pharmacology and experimental therapeutics,(3),736-744.
    显示于类别:[生物科技學系] 期刊論文


    档案 描述 大小格式浏览次数


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