Ginsenoside Rb1 improves cardiac function and remodeling in heart failure

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  • Zheng Xian
    Graduate School, Liaoning University of Traditional Chinese Medicine, 79 Chongshan East Road, Shenyang 110847, P.R. China
  • Wang Shuai
    First Department of Cardiology, The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, 33 Beiling Avenue, Shenyang 110032, P.R. China
  • Zou Xiaoming
    Graduate School, Liaoning University of Traditional Chinese Medicine, 79 Chongshan East Road, Shenyang 110847, P.R. China
  • Jing Yating
    First Department of Cardiology, The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, 33 Beiling Avenue, Shenyang 110032, P.R. China
  • Yang Ronglai
    First Department of Cardiology, The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, 33 Beiling Avenue, Shenyang 110032, P.R. China
  • Li Siqi
    Standardization Office, The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, 33 Beiling Avenue, Shenyang 110032, P.R. China
  • Wang Fengrong
    First Department of Cardiology, The Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, 33 Beiling Avenue, Shenyang 110032, P.R. China

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<p> We investigated the effect of ginsenoside Rb1 on cardiac function and remodeling in heart failure (HF). Four weeks after HF induction, the rats were administrated with ginsenoside Rb1 (35 and 70 mg/kg) and losartan (4.5 mg/kg) for 8 weeks. Losartan was used as a positive control. Cardiac function was assessed by measuring hemodynamic parameters. Histological changes were analyzed by HE and Masson’s trichrome staining. Cardiac hypertrophy, fibrosis, mitochondrial membrane potential and glucose transporter type 4 (GLUT4) levels were evaluated. In the present study, high dose of (H−) ginsenoside Rb1 decreased heart rate, improved cardiac function and alleviated histological changes induced by HF. H-ginsenoside Rb1 attenuated cardiac hypertrophy and myocardial fibrosis by decreasing left ventricular (LV) weight/heart weight ratio and cardiomyocyte cross-sectional area and reducing the levels of atrial natriuretic factor (ANF), β-myosin heavy chain (β-MHC), periostin, collagen I, Angiotensin II (Ang II), Angiotensin converting enzyme (ACE) and Ang II type 1 (AT1) receptor. Moreover, H-ginsenoside Rb1 decreased mitochondrial membrane potential and enhanced the translocation of GLUT4 to plasma membrane. The TGF-β1/Smad and ERK signaling pathways were inhibited and the Akt pathway was activated. These findings suggest that ginsenoside Rb1 might restore cardiac/mitochondrial function, increase glucose uptake and protect against cardiac remodeling via the TGF-β1/Smad, ERK and Akt signaling pathways.</p>

Journal

  • Experimental Animals

    Experimental Animals 66 (3), 217-228, 2017

    Japanese Association for Laboratory Animal Science

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