title: [Study on the expression of activin-A in myocardial ischemia postconditioning].
abstract: OBJECTIVE
  To analyze the relationship between the hydroxy free radical (* OH) and the activity of lactate dehydrogenase (LDH) and to study the potential role of activin-A in myocardial ischemia postconditioning for the protection of myocardium.
  
  
  METHODS
  Forty healthy adult Sprague-Dawley rats (gender unconcerned) were randomly divided into four different groups (n = 10 in each group): sham-operation, ischemia (I), ischemia/reperfusion (I/R) and ischemia postconditioning (postcon). In anesthetized open-chest rats, the left anterior descending artery (LAD) was ligated. Sham operation: the surgical procedure was identical to other groups, but the LAD was ligated for only 30 min, and not occluded. Ischemia: the LAD was occluded for 30 min; Ischemia/reperfusion: the LAD was occluded for 30 min and reperfused for 1 h; Postconditioning: after LAD occlusion for 30 min, at the start of reperfusion, three cycles of 30 s reperfusion and 30 s LAD re-occlusion preceded the 1h of reperfusion. The expression of activin-A in myocardium was detected by ELISA in all groups. The ability of suppression on the hydroxy free radical (* OH) and the activity of lactate dehydrogenase (LDH) in myocardium taken from each group were measured by spectrophotometer.
  
  
  RESULTS
  Compared with the sham-operated group, the expression of activin-A was significantly elevated in ischemia, ischemia/reperfusion and postconditiong groups, with the highest in the ischemia/reperfusion group. And postconditioning significantly decreased the expression of activin-A in the ischemia/ reperfusion injured myocardium [(343.05 +/- 25.8) microg/mg protein vs (470.6 +/- 33.1) microg/mg protein, P < 0.05]. The expression of activin-A was negatively correlated with the ability of suppression on the hydroxy free radical and LDH separately.
  
  
  CONCLUSIONS
  The result indicated that activin-A was involved in myocardial ischemia/reperfusion injury, and down-regulation of activin-A might be one of the cardioprotective mechanisms of postconditioning.
authors.affiliation: Department of Cardiology, West China Hospital, Sichuan University, Chengdu 610041, China.
authors.forename: Ling-Jun
authors.initials: LJ
authors.lastname: Zhang
authors.forename: He
authors.initials: H
authors.lastname: Huang
authors.forename: Ping-Xi
authors.initials: PX
authors.lastname: Pan
authors.forename: Xiao-Jing
authors.initials: XJ
authors.lastname: Liu
authors.forename: Wen-Chao
authors.initials: WC
authors.lastname: Wu
authors.forename: Hua
authors.initials: H
authors.lastname: Fu
mesh_terms: D000818:Animals; D005260:Female; D017665:Hydroxyl Radical / Q000378:metabolism; D028322:Inhibin-beta Subunits / Q000235:genetics / Q000378:metabolism*; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: C103008:inhibin beta A subunit; D017665:Hydroxyl Radical; D028322:Inhibin-beta Subunits; D007770:L-Lactate Dehydrogenase