title: The ginsenoside Rg1 prevents transverse aortic constriction-induced left ventricular hypertrophy and cardiac dysfunction by inhibiting fibrosis and enhancing angiogenesis.
abstract: 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.
authors.affiliation: *Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China.
authors.forename: Yao-Jun
authors.initials: YJ
authors.lastname: Zhang
authors.forename: Xin-Lei
authors.initials: XL
authors.lastname: Zhang
authors.forename: Ming-Hui
authors.initials: MH
authors.lastname: Li
authors.forename: Javaid
authors.initials: J
authors.lastname: Iqbal
authors.forename: Christos V
authors.initials: CV
authors.lastname: Bourantas
authors.forename: Jing-Jing
authors.initials: JJ
authors.lastname: Li
authors.forename: Xing-Yu
authors.initials: XY
authors.lastname: Su
authors.forename: Takashi
authors.initials: T
authors.lastname: Muramatsu
authors.forename: Nai-Liang
authors.initials: NL
authors.lastname: Tian
authors.forename: Shao-Liang
authors.initials: SL
authors.lastname: Chen
mesh_terms: D043925:Angiogenesis Inducing Agents; D000818:Animals; D015153:Blotting, Western; D003251:Constriction, Pathologic / Q000150:complications* / Q000517:prevention & control*; D004789:Enzyme Activation / Q000187:drug effects; D005355:Fibrosis; D036145:Ginsenosides / Q000494:pharmacology*; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology* / Q000517:prevention & control*; D051793:Hypoxia-Inducible Factor 1 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D009206:Myocardium / Q000473:pathology; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D051058:Oncogene Protein v-akt / Q000378:metabolism; D016612:Paraffin Embedding; D011347:Procollagen / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D014463:Ultrasonography; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000209:etiology* / Q000517:prevention & control*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
chemical_list: D043925:Angiogenesis Inducing Agents; D036145:Ginsenosides; D051793:Hypoxia-Inducible Factor 1; D011347:Procollagen; D042461:Vascular Endothelial Growth Factor A; D051058:Oncogene Protein v-akt; D048051:p38 Mitogen-Activated Protein Kinases; C035054:ginsenoside Rg1