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    標題: Tanshinone-induced ERs suppresses IGFII activation to alleviate Ang II-mediated cardiac hypertrophy
    作者: Chen, Ya-Fang
    Lee, Nien-Hung
    Pai, Pei-Ying
    Chung, Li-Chin
    Shen, Chia-Yao
    Rajendran, Peramaiyan
    Chen, Yu-Feng
    Chen, Ray-Jade
    Viswanadha, Vijaya Padma
    Kuo, Wei-Wen
    Huang, Chih-Yang
    貢獻者: China Med Univ, Grad Inst Basic Med Sci
    Taichung Vet Gen Hosp, Dept Obstet & Gynecol
    China Med Univ Hosp, Div Cardiol
    Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm
    MeiHo Univ, Dept Nursing
    Armed Force Taichung Gen Hosp, Dept Internal Med, Div Cardiol
    Taipei Med Univ, Sch Med, Coll Med, Dept Surg
    Bharathiar Univ, Dept Biotechnol, Coimbatore
    China Med Univ, Dept Biol Sci & Technol
    China Med Univ, Sch Chinese Med
    Asia Univ, Dept Hlth & Nutr Biotechnol
    關鍵字: Angiotensin II
    estrogen receptors
    H9c2 cardiomyoblasts
    hypertrophy
    IGF-2R
    tanshinone IIA
    日期: 2017
    上傳時間: 2018-11-30 15:53:54 (UTC+8)
    出版者: Taylor & Francis Ltd
    摘要: Cardiomyopathy involves changes in myocardial ultrastructure and cardiac hypertrophy. Angiotensin II (AngII) has previously been shown to stimulate the expression of IGF-2 and IGF-2R in H9c2 cardiomyoblasts and increase of blood pressure, and cardiac hypertrophy. Estrogen receptors (ERs) exert protective effects, such as anti-hypertrophy in cadiomyocytes. Tanshinone IIA (TSN), a main active ingredient from a Chinese medical herb, Salvia miltiorrhiza Bunge (Danshen), was shown to protect cardiomyocytes hypertrophy by different stress signals. We aimed to investigate whether TSN protected H9c2 cardiomyocytes from AngII-induced activation of IGF-2R pathway and hypertrophy by mediating through ERs. AngII resulted in H9c2 cardiomyoblast hypertrophy and increased inflammatory molecular markers. These were down-regulated by TSN via estrogen receptors. AngII resulted in elevation in MAPKs, IGF-2R and hypertrophic protein markers. These, again, were reduced by addition of the phytoestrogen with activation of ERs. Finally, AngII induced phosphorylation of heat shock factor-1 (HSF1) and decreased sirtuin-1 (SIRT1). In addition, AngII also caused an increase in distribution of IGF-2R molecules on cell membrane. In contrast, TSN reduced HSF1 phosphorylation and cell surface IGF-2R while elevating SIRT1 via ERs. TSN was capable of attenuating AngII-induced IGF-2R pathway and hypertrophy through ERs in H9c2 cardiomyoblast cells.
    Appears in Collections:[醫務管理系(所)] 期刊論文

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