English  |  正體中文  |  简体中文  |  Items with full text/Total items : 90453/105671 (86%)
Visitors : 16038924      Online Users : 104
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version


    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16149


    Title: Butein Up-Regulates the Expression of the π Class of Glutathione S-Transferase in Rat Primary Hepatocytes through the ERK/AP-1 Pathway
    Authors: 張竣維;Hebron, C.Chang
    Contributors: 生物科技學系
    Keywords: "Butein;π class of glutathione S-transferase;extracellular signal-regulated kinase;activator protein-1;rat primary hepatocytes"
    Date: 2010
    Issue Date: 2012-11-23 17:09:12 (UTC+8)
    Abstract: "Induction of phase II enzymes is an important mechanism of chemoprevention. Here we compared the
    effects of chalcones on the expression of the π class of glutathione S-transferase (GSTP) in rat primary
    hepatocytes. Hepatocytes were treated with 10 or 25 μM of phloretin or butein for 24 h. Both butein and
    phloretin dose-dependently increased GSTP protein expression, and the induction potency of butein was
    stronger than that of phloretin. The increase in GSTP mRNA in cells treated with 25 μM of phloretin and
    butein was 107% and 211%, respectively (P < 0.05). Butein increased GST enzyme activity by 27%
    compared with that in the control cells (P < 0.05). In contrast, phloretin had no significant effect on GST
    enzyme activity. The pTA-luciferase reporter construct with the rat -2.7 kb GSTP promoter region was
    transiently transfected into Clone 9 liver cells, and the luciferase activity in butein-treated cells was 1.1-fold
    higher than that in control cells (P < 0.05). GSTP enhancer 1 (GPE1) deletion abolished the induction of
    reporter activity by butein. The phosphorylation of extracellular signal-regulated kinase (ERK), but not of
    c-Jun NH2-terminal kinase (JNK) and p38, was stimulated in the presence of butein. Pretreatment with
    PD98059, an ERK inhibitor, alleviated the increase in activator protein-1 (AP-1)-DNA binding activity and
    also the activation of GSTP protein expression by butein. Moreover, c-Jun is likely to bind to the GPE1.
    Silencing of ERK2 by siRNA gene knockdown reduced the butein-induced expression of GSTP. In
    conclusion, the increased GSTP expression by butein is likely related to the ERK-AP-1 pathway."
    Relation: JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
    Appears in Collections:[生物科技學系] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML253View/Open


    All items in ASIAIR are protected by copyright, with all rights reserved.


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