title: Daidzein administration in vivo reduces myocardial injury in a rat ischemia/reperfusion model by inhibiting NF-kappaB activation.
abstract: OBJECTIVE
  We tested the hypothesis that daidzein may reduce myocardial damage by both inhibiting the release of cytokines and limiting the nuclear translocation of NF-kappaB.
  
  
  METHODS
  Male Sprague-Dawley rats were anesthetized, and the left anterior descending coronary artery (LAD) was ligated for 25 min. Twenty-four hours after reperfusion was established, the hemodynamics and infarct size were examined.
  
  
  RESULTS
  Treatment with daidzein (10 mg/kg, i.p.) 1 h prior to the ischemia/reperfusion procedure (I/R) reduced the infarct size by 52.8% (P<0.05). Daidzein also significantly improved I/R-induced myocardial contractile dysfunction by improving the left ventricular diastolic pressure and the positive and negative maximal values of the first derivative of the left ventricular pressure. In addition, daidzein reduced the plasma levels of TNF-alpha and IL-6 in I/R rats and decreased malondialdehyde levels, myeloperoxidase activity, catalase activity and neutrophil infiltration in I/R rat myocardium. Interestingly, daidzein inhibited I/R-induced myocardial apoptosis by decreasing DNA strand breaks and cleaved caspase-3 activity. Furthermore, daidzein inhibited both the nuclear translocation of NF-kappaB in I/R rat hearts and the H(2)O(2)-induced activation of NF-kappaB-luciferase activity in human umbilical vein endothelial cells.
  
  
  CONCLUSIONS
  This study reveals that the administration of daidzein in vivo attenuates I/R-induced myocardial damage via inhibition of NF-kappaB activation, which in turn may suppress inflammatory cytokine expression.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, School of Medicine, Gyeongsang National University, Jinju, 660-751, Republic of Korea. masa-t@msic.med.osaka-cu.ac.jp
authors.forename: Jong Woo
authors.initials: JW
authors.lastname: Kim
authors.forename: Yong Chun
authors.initials: YC
authors.lastname: Jin
authors.forename: Young Min
authors.initials: YM
authors.lastname: Kim
authors.forename: Sangho
authors.initials: S
authors.lastname: Rhie
authors.forename: Hye Jung
authors.initials: HJ
authors.lastname: Kim
authors.forename: Han Geuk
authors.initials: HG
authors.lastname: Seo
authors.forename: Jae Heun
authors.initials: JH
authors.lastname: Lee
authors.forename: Yeong Lae
authors.initials: YL
authors.lastname: Ha
authors.forename: Ki Churl
authors.initials: KC
authors.lastname: Chang
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D007529:Isoflavones / Q000494:pharmacology* / Q000627:therapeutic use; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015850:Interleukin-6; D007529:Isoflavones; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; C004742:daidzein