title: Sulfur dioxide preconditioning increases antioxidative capacity in rat with myocardial ischemia reperfusion (I/R) injury.
abstract: BACKGROUND
  The study was designed to explore if sulfur dioxide (SO2) preconditioning increased antioxidative capacity in rat with myocardial ischemia reperfusion (I/R) injury.
  
  
  METHODS
  The myocardial I/R model was made by left coronary artery ligation for 30min and reperfusion for 120min in rats. Myocardial infarct size and plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activities, plasma superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and glutathione (GSH) changes were detected for the rats. The contents of myocardial hydrogen sulfide (H2S) and nitric oxide (NO) were measured. Myocardial protein expressions of SOD1, SOD2, cystathionine γ-lyase (CSE) and iNOS were tested using Western blot.
  
  
  RESULTS
  Myocardial infarction developed and plasma CK and LDH activities were significantly increased in I/R group compared with those in control group, but SO2 preconditioning significantly reduced myocardial infarct size, and plasma CK and LDH activities. SO2 preconditioning successfully increased plasma SOD, GSH and GSH-Px levels and myocardial SOD1 protein expression, but decreased MDA level in rats of I/R group. Compared with controls, the myocardial H2S level and CSE expression were decreased after I/R, but myocardial NO level and iNOS expression were increased. With the treatment of SO2, myocardial H2S level and CSE expression were increased, but myocardial NO level and iNOS expression were decreased compared with those in I/R group.
  
  
  CONCLUSIONS
  SO2 preconditioning could significantly reduce I/R-induced myocardial injury in vivo in association with increased myocardial antioxidative capacity, upregulated myocardial H2S/CSE pathway but downregulated NO/iNOS pathway.
authors: Department of Pediatrics, Peking University First Hospital, Beijing 100034, PR China.
authors: Hong fang
authors: Hf
authors: Jin
authors: Yuan
authors: Y
authors: Wang
authors: Xin bao
authors: Xb
authors: Wang
authors: Yan
authors: Y
authors: Sun
authors: Chao shu
authors: Cs
authors: Tang
authors: Jun bao
authors: Jb
authors: Du
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D003402:Creatine Kinase / Q000378:metabolism; D003542:Cystathionine gamma-Lyase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013458:Sulfur Dioxide / Q000494:pharmacology*; D013482:Superoxide Dismutase / Q000378:metabolism; D000072105:Superoxide Dismutase-1
chemical_list: D000975:Antioxidants; D013458:Sulfur Dioxide; D009569:Nitric Oxide; D007770:L-Lactate Dehydrogenase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; C000606292:Sod1 protein, rat; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D003402:Creatine Kinase; D003542:Cystathionine gamma-Lyase; D005978:Glutathione