title: [Effect of erythropoietin combined with granulocyte-colony stimulating factor in the treatment of acute myocardial infarction in rats].
abstract: OBJECTIVE
  To evaluate the effects of erythropoietin (EPO) combined with granulocyte-colony stimulating factor (G-CSF) on left ventricular function and ventricular remodeling after acute myocardial infarction (AMI) and investigate the possible mechanism.
  
  
  METHODS
  The experimental design consisted of 5 groups of rats, namely the sham, myocardial infarction (MI) model, MI with EPO treatment, MI with G-CSF treatment, and MI with EPO plus G-CSF treatment groups. Apoptosis of the cardiomyocytes was detected by TUNEL staining, and HE staining, Masson trichrome staining, scarlatinum staining, and VIII agent staining were used to evaluate the survival, scar collagen deposition, and angiogenic effects. The cardiac structure and function of the rats after the treatments were assessed by echocardiography and hemodynamic examination.
  
  
  RESULTS
  Echocardiography indicated that LVEF and FS were improved in all the intervention groups 7 days after MI, and the rats in EPO plus G-CSF treatment group showed the most obvious reduction of LVESD and LVESV (P<0.01). On day 28 after MI, all the intervention groups showed improvements in LVEF, FS, LVESD, LVEDD, LVESV and LVEDV, which were especially obvious in the combined treatment group; the interventions, especially the combined treatment, also resulted in decreased LVEDP and increased LVSP and +dP/dtmax. On day 1 after MI, the number of apoptotic cells was significantly greater in the MI model group than in EPO and G-CSF groups, and was the fewest in the combined treatment group (P<0.01). On day 28, the number of new vessels increased and the scar and collagen deposition reduced in the EPO and G-CSF groups, and these changes were more obvious in the combined treatment group.
  
  
  CONCLUSIONS
  EPO combined with G-CSF can prevent left ventricular remodeling and improve cardiac systolic and diastolic functions by inhibiting cardiomyocyte apoptosis, reducing tissue collagen deposition and inducing neovascularisation.
authors.affiliation: Department of Cardiology, General Hospital of PLA, Beijing 100853, China. fuzhenh@sina.com
authors.forename: Zhen-hong
authors.initials: ZH
authors.lastname: Fu
authors.forename: Wei
authors.initials: W
authors.lastname: Dong
authors.forename: Lu-yue
authors.initials: LY
authors.lastname: Gai
authors.forename: Fan
authors.initials: F
authors.lastname: Wang
authors.forename: Rui
authors.initials: R
authors.lastname: Ding
authors.forename: Yun-dai
authors.initials: YD
authors.lastname: Chen
mesh_terms: D000818:Animals; D004359:Drug Therapy, Combination; D004921:Erythropoietin / Q000627:therapeutic use*; D005260:Female; D016179:Granulocyte Colony-Stimulating Factor / Q000627:therapeutic use*; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D016277:Ventricular Function, Left / Q000502:physiology; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D004921:Erythropoietin; D016179:Granulocyte Colony-Stimulating Factor