title: The PI3K/Akt pathway mediates the protection of SO(2) preconditioning against myocardial ischemia/reperfusion injury in rats.
abstract: OBJECTIVE
  To explore the mechanisms underlying the protection by SO2 preconditioning against rat myocardial ischemia/reperfusion (I/R) injury.
  
  
  METHODS
  Male Wistar rats underwent 30-min left coronary artery ligation followed by 120-min reperfusion. An SO2 donor (1 μmol/kg) was intravenously injected 10 min before the ischemia, while LY294002 (0.3 mg/kg) was intravenously injected 30 min before the ischemia. Plasma activities of LDH and CK were measured with an automatic enzyme analyzer. Myocardial infarct size was detected using Evans-TTC method. The activities of caspase-3 and -9 in myocardium were assayed using a commercial kit, and the levels of p-Akt, Akt, PI3K and p-PI3K were examined with Western blotting.
  
  
  RESULTS
  Pretreatment with SO2 significantly reduced the myocardial infarct size and plasma LDH and CK activities, as well as myocardial caspase-3 and -9 activities in the rats. Furthermore, the pretreatment significantly increased the expression levels of myocardial p-Akt and p-PI3K p85. Administration of the PI3K inhibitor LY294002 blocked all the effects induced by SO2 pretreatment.
  
  
  CONCLUSIONS
  The results suggest that the PI3K/Akt pathway mediates the protective effects of SO2 preconditioning against myocardial I/R injury in rats.
authors.affiliation: Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
authors.forename: Man-man
authors.initials: MM
authors.lastname: Zhao
authors.forename: Jin-yan
authors.initials: JY
authors.lastname: Yang
authors.forename: Xin-bao
authors.initials: XB
authors.lastname: Wang
authors.forename: Chao-shu
authors.initials: CS
authors.lastname: Tang
authors.forename: Jun-bao
authors.initials: JB
authors.lastname: Du
authors.forename: Hong-fang
authors.initials: HF
authors.lastname: Jin
mesh_terms: D000818:Animals; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D053453:Caspase 9 / Q000235:genetics / Q000378:metabolism; D002867:Chromones / Q000494:pharmacology; D003331:Coronary Vessels / Q000378:metabolism; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D009025:Morpholines / Q000494:pharmacology; D009203:Myocardial Infarction / Q000235:genetics / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000201:enzymology / Q000235:genetics / Q000378:metabolism* / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism*; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction; D013458:Sulfur Dioxide / Q000494:pharmacology*
chemical_list: D002867:Chromones; D009025:Morpholines; D013458:Sulfur Dioxide; C085911:2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D053148:Caspase 3; D053453:Caspase 9