title: Ischemic postconditioning through percutaneous transluminal coronary angioplasty in pigs:  roles of PI3K activation.
abstract: BACKGROUND
  Ischemic postconditioning (IPOC) has been suggested to reduce ischemic reperfusion injury. It remains unclear whether the activation of phosphatidylinositol 3 kinase (PI3K)/Akt is a causal mechanism in the cardioprotection afforded by IPOC, which was examined in the model of percutaneous transluminal coronary angioplasty (PTCA) minipigs.
  
  
  RESULTS
  Minipigs underwent 45-min occlusion of the left anterior descending artery and 24-h reperfusion by PTCA. Postconditioning was elicited by three cycles of 30-s reperfusion followed by 30-s ischemia at the onset of reperfusion. Infarct size was determined by triphenyl tetrazolium chloride staining after 24-h reperfusion, and mRNA and protein expression levels of PI3K were ascertained by reverse transcriptase-PCR and western-blot analysis in biopsies. Infarct size was significantly reduced and myocardial PI3K (Akt and GSK-3β) phosphorylation was significantly increased with IPOC treatment compared with ischemic reperfusion. The administration of the PI3K inhibitor wortmannin (30 µg/kg) attenuated the protection of IPOC in the infarct size and decreased the expression of Akt and GSK-3β phosphorylation compared with IPOC. IPOC had no impact on mRNA expression of AKT and GSK-3β.
  
  
  CONCLUSIONS
  Our findings show that IPOC is capable of protecting the myocardium against IR injury in the PTCA minipig model. The PI3K/Akt-signaling pathway is involved in the cardioprotective effect of IPOC.
authors.affiliation: Department of Cardiovascular Disease, Xiyuan Hospital, China Academy of Chinese Medicine Sciences, Beijing, China.
authors.forename: Xiao-Juan
authors.initials: XJ
authors.lastname: Ma
authors.forename: Hui-Jun
authors.initials: HJ
authors.lastname: Yin
authors.forename: Chun-Yu
authors.initials: CY
authors.lastname: Guo
authors.forename: Yue-Rong
authors.initials: YR
authors.lastname: Jiang
authors.forename: Jing-Shang
authors.initials: JS
authors.lastname: Wang
authors.forename: Da-Zhuo
authors.initials: DZ
authors.lastname: Shi
mesh_terms: D000730:Androstadienes / Q000627:therapeutic use; D015906:Angioplasty, Balloon, Coronary; D000818:Animals; D015153:Blotting, Western; D017023:Coronary Angiography; D017931:DNA Primers / Q000737:chemistry; D005260:Female; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D057775:Ischemic Postconditioning / Q000379:methods*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000201:enzymology / Q000517:prevention & control*; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010766:Phosphorylation / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000502:physiology; D013552:Swine; D013556:Swine, Miniature; D000077191:Wortmannin
chemical_list: D000730:Androstadienes; D017931:DNA Primers; D038362:Glycogen Synthase Kinase 3; D000071679:Glycogen Synthase Kinase 3 beta; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D051057:Proto-Oncogene Proteins c-akt; D012333:RNA, Messenger; D000077191:Wortmannin