title: Effect and mechanism of panaxoside Rg1 on neovascularization in myocardial infarction rats.
abstract: OBJECTIVE
  To investigate the effects and mechanisms of panaxoside Rg1 on the new vessel formation in acute myocardial infarction (AMI) rats.
  
  
  METHODS
  The AMI model of male Sprague-Dawley (SD) rats was established, and rats were randomly divided into the AMI model group, the treatment group of panaxoside Rg1, the placebo group and the treatment group of panaxoside Rg1 plus rapamycin. Cardiac creatases were determined with 1 mL blood drawn from vena caudalis of the rats 48 h after the model was successfully made. After 4 weeks, Evans blue was injected into the aorta roots of the rats, and then, red tetrazoline was dyed again and the myocardial infarction area was evaluated. The microvessel density (MVD) of infarction area was determined by the immunohistochemistry of CD31; enzyme-linked immunosorbent assay (ELISA) was used to detect the protein content of CD31 and hypoxia inducible factor-1alpha (HIF-1alpha) of the infarction area.
  
  
  RESULTS
  The MVD in the infarction area and the contents of CD31 and HIF-1alpha in the Rg1 treatment group were higher than those in the AMI model group significantly (P<0.05). The cardiac creatase and infarction area were lower in the Rg1 treatment group than those in the AMI model group significantly (P<0.05). The above effects, however, disappeared when rapamycin, the antagonist of mammalian target of rapamycin (mTOR), was administered simultaneously.
  
  
  CONCLUSIONS
  Panaxoside Rg1 could increase the expression of HIF-1alpha and CD31 of myocardium and stimulate the angiogenesis. The above mentioned role of panaxoside Rg1 might be related to the excitation of mTOR receptor.
authors.affiliation: Department of Cardiac Surgery, the First Affiliated Hospital, China Medical University, Shenyang (110001), China.
authors.forename: Xiao-dong
authors.initials: XD
authors.lastname: Wang
authors.forename: Tian-xiang
authors.initials: TX
authors.lastname: Gu
authors.forename: En-Yi
authors.initials: EY
authors.lastname: Shi
authors.forename: Chun-mao
authors.initials: CM
authors.lastname: Lu
authors.forename: Chun
authors.initials: C
authors.lastname: Wang
mesh_terms: D000818:Animals; D002452:Cell Count; D003097:Collateral Circulation / Q000187:drug effects; D004353:Drug Evaluation, Preclinical; D036145:Ginsenosides / Q000008:administration & dosage / Q000494:pharmacology*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism / Q000502:physiology; D008297:Male; D055806:Microvessels / Q000473:pathology; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D018919:Neovascularization, Physiologic / Q000187:drug effects*; D010919:Placebos; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism / Q000502:physiology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D020123:Sirolimus / Q000008:administration & dosage / Q000494:pharmacology; D058570:TOR Serine-Threonine Kinases
chemical_list: D036145:Ginsenosides; C497444:Hif1a protein, rat; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D047908:Intracellular Signaling Peptides and Proteins; D010919:Placebos; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C546845:mTOR protein, rat; D017346:Protein Serine-Threonine Kinases; D058570:TOR Serine-Threonine Kinases; C035054:ginsenoside Rg1; D020123:Sirolimus
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