title: [Protective effect and mechanism of pharmacologic preconditioning induced by sodium ferulate on primary cultured myocardial cell injury by anoxia/reoxygenation].
abstract: OBJECTIVE
  To study the preconditioning effects and mechanism of action of sodium ferulate (SF) on primary cultured myocardial cell injury induced by anoxia/reoxygenation.
  
  
  METHODS
  Cultured myocardial cells of neonatal SD rats were randomly divided into ten groups: control group: without any treatment; anoxia/reoxygenation group (A/R), reoxygenation of 1 h following anoxia of 3 h; anoxia preconditioning group (AP), reoxygenation of 30 mins following anoxia of 30 mins, three times before the same procedure as group A/R; SF preconditioning groups, 20 mins of SF (1.68, 0.42, 0.105 mmol x L(-1) in final concentration) preconditioning followed by 10 mins wash out before A/R; K+ATP channel blocker group, NOS inhibitor group and PKC inhibitor group, adding gliberclamide, L-NAME, ploymyxin B at final concentration of 12 g x mL(-1), 50 micromol x L(-1), 50 micromol x L(-1), to culture medium respectively 10 min before the same procedures as SF preconditioning group (1.68 mmol x L(-1)). Myocardial cells pulse rate and rhythm, myocyte viability, the activity of LDH and CK in culture, the contents of intracelluar MDA, LD in myocardial cells, the activity of SOD and GSH-Px of the cultured myocardial cell were measured at the end of experiment.
  
  
  RESULTS
  Compared with control group, anoxia/reoxygenation caused great increases of levels of LDH, CK, MDA and LD (P < 0.01), decreases of myocardial cells pulse rate, cell viability, SOD and GSH-Px (P < 0.01); SF preconditioning significantly attenualed these increases and decreases. Glib, L-NAME, and Ploy B partly abolished the effects of SF preconditioning.
  
  
  CONCLUSIONS
  SF preconditioning is effective in protecting myocardial cells from anoxia injury. The cardioprotective effect of SF preconditioning is produced by multiple factors.
authors.affiliation: Department of Pharmacology, Jiangxi Medical College, Nanchang 330006, China. fuyingjun@163.com
authors.forename: Ying-jun
authors.initials: YJ
authors.lastname: Fu
authors.forename: Ming
authors.initials: M
authors.lastname: He
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D003373:Coumaric Acids / Q000494:pharmacology*; D003402:Creatine Kinase / Q000378:metabolism; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D019157:Ischemic Preconditioning, Myocardial; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D017202:Myocardial Ischemia / Q000150:complications; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D003373:Coumaric Acids; D008315:Malondialdehyde; C004999:ferulic acid; D007770:L-Lactate Dehydrogenase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D003402:Creatine Kinase