title: The protective effect of Egr-1 antisense oligodeoxyribonucleotide on myocardial injury induced by ischemia-reperfusion and hypoxia-reoxygenation.
abstract: OBJECTIVE
  Our previous studies have shown that myocardial ischemia-reperfusion (I/R) injury is related closely with early growth response (Egr)-1 overexpression. The present study is to confirm thoroughly the effects of Egr-1 on the occurrance and development of myocardial I/R injury.
  
  
  METHODS
  The Sprague-Dawley rat myocardial I/R model and cultured cardiomyocyte hypoxia-reoxygenation (H/R) model were established. The synthesized Egr-1 antisense oligodeoxyribonucleotide (AS-ODN) was transfected into myocardial tissues and cells. Hemodynamic parameters, myeloperoxidase (MPO), cardiac troponin I (cTnI), tumor necrosis factor-alpha (TNF-alpha), morphology, spontaneous beat and cell viability were measured to assess the degree of injury and inflammation of myocardial tissues and cells.
  
  
  RESULTS
  In vivo, Egr-1 AS-ODN significantly attenuated injury and inflammation of myocardial tissues caused by I/R evidenced by the amelioration of hemodynamics and the reduction in MPO activity. In vitro, Egr-1 AS-ODN significantly relieved injury and inflammation of cultured cardiomyocyte caused by H/R evidenced by the improvement in morphology, structure and beat as well as the decrease in leakage of cTnI and release of TNF-alpha from cultured cardiomyocyte.
  
  
  CONCLUSIONS
  These data suggest that Egr-1 plays a vital role in the pathogenesis of myocardial I/R injury and Egr-1 AS-ODN could protect the myocardium from I/R injury.
authors.affiliation: Department of Pharmacology, Shantou University Medical College, Shantou, Guangdong, China.
authors.forename: Yanmei
authors.initials: Y
authors.lastname: Zhang
authors.forename: Ganggang
authors.initials: G
authors.lastname: Shi
authors.forename: Jinhong
authors.initials: J
authors.lastname: Zheng
authors.forename: Yanqiu
authors.initials: Y
authors.lastname: Lv
authors.forename: Ping
authors.initials: P
authors.lastname: Gao
authors.forename: Zhanqin
authors.initials: Z
authors.lastname: Huang
authors.forename: Fenfei
authors.initials: F
authors.lastname: Gao
authors.forename: Yanqiong
authors.initials: Y
authors.lastname: Zhou
mesh_terms: D000818:Animals; D015687:Cell Hypoxia / Q000187:drug effects; D048430:Cell Shape / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003470:Culture Media; D051766:Early Growth Response Protein 1 / Q000378:metabolism*; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000201:enzymology / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000473:pathology; D020319:Oligodeoxyribonucleotides, Antisense / Q000378:metabolism / Q000494:pharmacology*; D010100:Oxygen / Q000494:pharmacology*; D009195:Peroxidase / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013347:Subcellular Fractions / Q000378:metabolism; D019210:Troponin I / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D003470:Culture Media; D051766:Early Growth Response Protein 1; C486110:Egr1 protein, rat; D020319:Oligodeoxyribonucleotides, Antisense; D020011:Protective Agents; D019210:Troponin I; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D010100:Oxygen