Green tea (-)-epigallocatechin gallate inhibits IGF-I and IGF-IIstimulation of 3T3-L1 preadipocyte mitogenesis via the 67-kDa laminin receptor, but not AMP-activated protein kinase pathway

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题名:	Green tea (-)-epigallocatechin gallate inhibits IGF-I and IGF-IIstimulation of 3T3-L1 preadipocyte mitogenesis via the 67-kDa laminin receptor, but not AMP-activated protein kinase pathway
作者:	高永旭;Ku, Hui‐Chen;Liu, Hang‐Seng;Hung, Pei‐Fang;Chen, Chia‐Lin;Liu, Hsien‐Chun;Chang, Hsin‐Huei;Tsuei, Yi‐Wei;Shih, Li‐Jane;Lin, Ching‐Ling;Lin, Chih‐Ming;Kao, Yung‐Hsi
贡献者:	生醫理工學院生命科學系
日期:	2012-04-01
上传时间:	2026-04-23 11:12:56 (UTC+8)
出版者:	Wiley-VCH Verlag;Wiley
摘要:	摘要： ScopeThis study investigated the pathways involved in epigallocatechin gallate (<jats:styled-content style="fixed-case">EGCG</jats:styled-content>) modulation of insulin‐like growth factor (<jats:styled-content style="fixed-case">IGF</jats:styled-content>)‐<jats:styled-content style="fixed-case">I</jats:styled-content>‐stimulated and <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">II</jats:styled-content>‐stimulated mitogenesis in 3<jats:styled-content style="fixed-case">T</jats:styled-content>3‐<jats:styled-content style="fixed-case">L</jats:styled-content>1 preadipocytes.Methods and resultsWe found that this process was dose and time dependent, and caused by suppression of <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">I</jats:styled-content>‐stimulated and <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">II</jats:styled-content>‐stimulated phosphorylation of p66<jats:styled-content style="fixed-case">S</jats:styled-content>hc and mitogen‐activated protein kinase (<jats:styled-content style="fixed-case">MAPK</jats:styled-content>) pathway proteins, including <jats:styled-content style="fixed-case">MEK</jats:styled-content>1 kinase (<jats:styled-content style="fixed-case">RAF</jats:styled-content>1), extracellular signal‐regulated protein kinase (<jats:styled-content style="fixed-case">ERK</jats:styled-content>) kinase (<jats:styled-content style="fixed-case">MEK</jats:styled-content>1), and ERK 1 and ERK 2 (<jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2), but not phospho‐<jats:styled-content style="fixed-case">J</jats:styled-content>un‐<jats:styled-content style="fixed-case">N</jats:styled-content>‐terminal kinase, protein kinase <jats:styled-content style="fixed-case">B</jats:styled-content>, p52<jats:styled-content style="fixed-case">S</jats:styled-content>hc, or p46<jats:styled-content style="fixed-case">S</jats:styled-content>hc. Furthermore, <jats:styled-content style="fixed-case">EGCG</jats:styled-content>inhibited the <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">I</jats:styled-content>‐stimulated phosphorylation of the <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">I</jats:styled-content> receptor‐beta (<jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">IR</jats:styled-content> β), the association of <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">IR</jats:styled-content>with the p66<jats:styled-content style="fixed-case">S</jats:styled-content>hc protein, and the <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">II</jats:styled-content>‐stimulated associations of the <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">II</jats:styled-content>receptor with <jats:styled-content style="fixed-case">G</jats:styled-content>αi‐2 and p66<jats:styled-content style="fixed-case">S</jats:styled-content>hc proteins, suggesting that <jats:styled-content style="fixed-case">EGCG</jats:styled-content>selectively affects particular types of <jats:styled-content style="fixed-case">S</jats:styled-content>hc and <jats:styled-content style="fixed-case">MAPK</jats:styled-content>family members. Pretreatment with antiserum against the <jats:styled-content style="fixed-case">EGCG</jats:styled-content>receptor (also known as the 67‐k<jats:styled-content style="fixed-case">D</jats:styled-content>a laminin receptor; 67<jats:styled-content style="fixed-case">LR</jats:styled-content>), but not with an adenosine monophosphate (<jats:styled-content style="fixed-case">AMP</jats:styled-content>)‐activated protein kinase (<jats:styled-content style="fixed-case">AMPK</jats:styled-content>) inhibitor, prevented the inhibitory actions of <jats:styled-content style="fixed-case">EGCG</jats:styled-content>on <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">I</jats:styled-content>‐ and <jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style="fixed-case">II</jats:styled-content>‐stimulated <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation and subsequent preadipocyte proliferation.ConclusionThe results of this study suggest that <jats:styled-content style="fixed-case">EGCG</jats:styled-content>mediates anti‐<jats:styled-content style="fixed-case">IGF</jats:styled-content>‐<jats:styled-content style= ... 出版者： Wiley 出版日期： 2012-04 出處： Molecular Nutrition & Food Research, 2012-04, Vol.56 (4), p.580-592 識別號： ISSN: 1613-4125 識別號： DOI: 10.1002/mnfr.201100438
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