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    Title: Ginsenoside Rh2 Improves Cardiac Fibrosis via PPAR delta-STAT3 Signaling in Type 1-Like Diabetic Rats
    Authors: Lo, Shih-Hsiang
    Hsu, Chao-Tien
    Niu, Ho-Shan
    Niu, Chiang-Shan
    Cheng, Juei-Tang
    Chen, Zhih-Cherng
    Contributors: Taipei City Hosp, Zhongxing Branch, Dept Internal Med
    Tzu Chi Univ Sci & Technol, Dept Nursing
    I Shou Univ, E DA Hosp, Dept Pathol
    Chi Mei Med Ctr, Dept Cardiol
    Chi Mei Med Ctr, Dept Med Res
    Chang Jung Christian Univ, Inst Med Sci
    Chia Nan Univ Pharm & Sci, Dept Pharm
    Keywords: ginsenoside Rh2
    PPAR delta
    cardiac fibrosis
    type-1 diabetes
    STZ rats
    Date: 2017-07
    Issue Date: 2018-11-30 15:52:21 (UTC+8)
    Publisher: Mdpi Ag
    Abstract: Ginsenoside Rh2 (Rh2) is an active principal ingredient contained in ginseng (Panax ginseng Meyer), a medicinal herb used to enhance health worldwide. The present study is designed to investigate the effect of Rh2 on myocardial fibrosis in diabetic rats. In a streptozotocin-induced model of type-1 diabetic rats (STZ-diabetic rats), the increased fasting blood glucose levels and heart weight/body weight (HW/BW) ratio were substantially alleviated by Rh2. Moreover, Rh2 improved cardiac performance in STZ-diabetic rats. Histological results from Masson staining showed that Rh2 attenuated cardiac fibrosis in STZ-diabetic rats. The effects of Rh2 were reversed by GSK0660 at a dose sufficient to inhibit peroxisome proliferator-activated receptor delta (PPAR delta) in STZ-diabetic rats. The role of PPAR delta was subsequently investigated in vitro. Rh2 restored the decreased PPAR delta expression level in high glucose-cultured cardiomyocytes. Moreover, increased protein levels of fibrotic signals, including signal transducer and activator of transcription 3 (STAT3), connective tissue growth factor (CCN2) and fibronectin, were reduced by Rh2 in high glucose-cultured cardiomyocytes. These effects of Rh2 were reversed by GSK0660 or siRNA specific for PPAR delta Taken together, PPAR delta activation may inhibit STAT3 activation to reduce CCN2 and fibronectin expression in diabetic rats with cardiac fibrosis. Moreover, Rh2 improves cardiac function and fibrosis by increasing PPAR delta signaling. Therefore, Rh2 is suitable to develop as an alternative remedy for cardiac fibrosis.
    Relation: International Journal of Molecular Sciences, v.18, n.7, pp.1364
    Appears in Collections:[Dept. of Pharmacy] Periodical Articles

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