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The Ginsenoside Rg1 Prevents Transverse Aortic ConstrictionInduced Left Ventricular Hypertrophy and Cardiac Dysfunction by Inhibiting Fibrosis and Enhancing Angiogenesis

Zhang, Yao-Jun MD*; Zhang, Xin-Lei MSc*; Li, Ming-Hui MD*; Iqbal, Javaid MRCP, PhD; Bourantas, Christos V. PhD; Li, Jing-Jing MSc*; Su, Xing-Yu BSc*; Muramatsu, Takashi MD, PhD; Tian, Nai-Liang MD*; Chen, Shao-Liang MD, PhD*

Journal of Cardiovascular Pharmacology: July 2013 - Volume 62 - Issue 1 - p 50–57
doi: 10.1097/FJC.0b013e31828f8d45
Original Article

Background: Ginsenoside Rg1, an important and active ingredient of Panax ginseng, has been shown to exert cardioprotective effects in vivo. The present study aimed to test the hypothesis that ginsenoside Rg1 attenuates cardiac dysfunction in a transverse aortic constriction (TAC)–induced left ventricular hypertrophy in vivo via proangiogenic and antifibrotic effects.

Methods: This study investigated the effects of ginsenoside Rg1 in a rat model of TAC-induced left ventricular hypertrophy. Cardiac function was assessed by echocardiography. The antifibrotic and proangiogenic effects were assessed by histopathology and mRNA expression of procollagen I, III, and vascular endothelial growth factor (VEGF) through quantitative real-time PCR. The expression of phosphorylation of Akt, p38 mitogen-activated protein kinase (MAPK), hypoxia inducible factor-1 (HIF-1), and VEGF proteins were examined by Western blotting.

Results: Ginsenoside Rg1 treatment significantly decreased TAC-induced myocardial fibrosis and left ventricular hypertrophy, and preserved cardiac function. Ginsenoside Rg1 administration enhanced angiogenesis by increasing the expression of HIF-1 and VEGF. These cardioprotective effects of ginsenoside Rg1 are partially related to the activation of phospho-Akt and inhibition of p38 MAPK.

Conclusions: Ginsenoside Rg1 exhibited protective effect against TAC-induced left ventricular hypertrophy and cardiac dysfunction, which is potentially associated with phospho-Akt activation and p38 MAPK inhibition.

*Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China;

Department of Cardiovascular Science, University of Sheffield, Sheffield, United Kingdom; and

Thoraxcenter, Erasmus Medical Center, Rotterdam, the Netherlands.

Reprints: Shao-Liang Chen, MD, PhD, Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, No. 68 Changle Road, Nanjing City 210006, China (e-mail: chmengx126@gmail.com).

Supported by the Research and Innovation Project for College Graduates of Jiangsu Province (2011, CXLX11_0719).

The authors report no conflicts of interest.

Y.J. Zhang, X.L. Zhang, and M.H. Li have contributed equally.

Received February 04, 2013

Accepted February 27, 2013

© 2013 by Lippincott Williams & Wilkins.