Document Detail


Ginsenoside-Rg1 enhances angiogenesis and ameliorates ventricular remodeling in a rat model of myocardial infarction.
MedLine Citation:
PMID:  21327539     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ginsenoside-Rg1 (Rg1) has been used in the traditional Chinese medicine for over 2,000 years. The present study was performed to test our hypothesis that Rg1 provides pro-angiogenic and anti-fibrotic benefits in the ischemic myocardium in a rat model of myocardial infarction. The expression of vascular endothelial growth factor (VEGF) and phosphorylation/activation of PI3K, Akt, and p38 MAPK signaling pathways were examined in human umbilical vein endothelial cells and in the myocardial samples of rats. In addition, the expression levels of TNF-α and collagen I level, the number of newly formed blood vessels, the extent of myocardial fibrosis, and left ventricular function were measured in vivo. Our results demonstrated that administration of Rg1 increased VEGF expression levels, activated PI3K/Akt, and inhibited p38 MAPK in vitro and in vivo. Furthermore, Rg1 increased the density of newly formed vessels, decreased TNF-α and collagen I expression levels and area of myocardial fibrosis, and improved left ventricle function in vivo. PI3K inhibitor LY294002 significantly attenuated Rg1-enhanced VEGF expression and capillary density. As well, inhibition of p38 MAPK slightly increased VEGF expression in vitro and in vivo, increased capillary density, and decreased TNF-α and collagen I expression levels and area of myocardial fibrosis in vivo. Rg1-induced activation of PI3K/Akt also contributed to the downregulation of p38 MAPK. Thus, Rg1 is effective in promoting angiogenesis and attenuating myocardial fibrosis, resulting in ameliorated left ventricular function. The possible mechanisms may involve activation of PI3K/Akt, inhibition of p38 MAPK, and cross talk between the two signaling pathways.
Authors:
Huiqiu Yin; Zhaoqiang Liu; Fuhai Li; Mei Ni; Bo Wang; Yun Qiao; Xinsheng Xu; Mei Zhang; Jidong Zhang; Huixia Lu; Yun Zhang
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Retracted Publication     Date:  2011-02-16
Journal Detail:
Title:  Journal of molecular medicine (Berlin, Germany)     Volume:  89     ISSN:  1432-1440     ISO Abbreviation:  J. Mol. Med.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-14     Completed Date:  2011-06-27     Revised Date:  2014-02-04    
Medline Journal Info:
Nlm Unique ID:  9504370     Medline TA:  J Mol Med (Berl)     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  363-75     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Coronary Vessels / drug effects*
Disease Models, Animal
Drugs, Chinese Herbal / pharmacology*
Endomyocardial Fibrosis / pathology
Gene Expression Regulation / drug effects
Ginsenosides / pharmacology*
Humans
Male
Myocardial Infarction / pathology*
Neovascularization, Physiologic / drug effects*
Proto-Oncogene Proteins c-akt / metabolism
Rats
Rats, Wistar
Signal Transduction / drug effects
Tumor Necrosis Factor-alpha / metabolism
Vascular Endothelial Growth Factor A / metabolism
Ventricular Remodeling / drug effects*
p38 Mitogen-Activated Protein Kinases / antagonists & inhibitors,  metabolism
Chemical
Reg. No./Substance:
0/Drugs, Chinese Herbal; 0/Ginsenosides; 0/Tumor Necrosis Factor-alpha; 0/Vascular Endothelial Growth Factor A; 22427-39-0/ginsenoside Rg1; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases
Comments/Corrections
Retraction In:
J Mol Med (Berl). 2013 May;91(5):645   [PMID:  23529760 ]

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