title: [Epigallocatechin-3-gallate Attenuates Myocardial Reperfusion Injury in Rats Through Activation of PI3K/Akt Signaling Pathway].
abstract: OBJECTIVE
  This study was designed to investigate whether epigallocatechin-3-gallate (EGCG) postconditioning protects the heart against ischemic-reperfusion injury (IRI), and to explore its potential mechanisms in a rat model.
  
  
  METHODS
  Male Wistar rats were subjected to myocardial ischemia (30 min) and reperfusion (up to 2 h) and the rats were divided into sham group (SO) group, ischemia-reperfusion (I/R) model group and EGCG group. EGCG group were treated with EGCG (10 mg/kg) via intravenous infusion 5 min before reperfusion. Electrocardiogram were applied to record ventricular arrhythmia frequency. The severity of myocardial injury [serum level of lactate dehydrogenase (LDH) and creatine kinase (CK), hematoxylineosin (HE) staining] and ventricular arrhythmia, and the serum levels of inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukins-6 (IL-6) and IL-8] were assessed with ELISA, electrocardiogram and Western blot respectively.
  
  
  RESULTS
  EGCG given before reperfusion could effectively reduce the serum level of LDH and CK and the incidence of ventricular arrhythmia (P < 0.05, respectively), improved the pathological damage. Meanwhile, EGCG could down-regulate the expression levels of TNF-α, IL-6, IL-8 in the myocardial tissue after IRI (P < 0.05, repectively). The expression levels of p-p85 and p-Akt in the EGCG group were significantly up-regulated compared to those in I/R group (P < 0.05, repectively).
  
  
  CONCLUSIONS
  EGCG-related anti-inflammatory action could attenuate rat myocardial IRI and this cardioprotective effect might be activated through the PI3K/Akt pathway.
authors.forename: Jia
authors.initials: J
authors.lastname: Hu
authors.forename: Jun
authors.initials: J
authors.lastname: Gu
authors.forename: Fei
authors.initials: F
authors.lastname: Xu
authors.forename: Hong-wei
authors.initials: HW
authors.lastname: Zhang
authors.forename: Kang-jun
authors.initials: KJ
authors.lastname: Fan
authors.forename: Chao-yi
authors.initials: CY
authors.lastname: Qin
authors.forename: Zheng
authors.initials: Z
authors.lastname: Xiao
authors.forename: Er-yong
authors.initials: EY
authors.lastname: Zhang
mesh_terms: D000818:Animals; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D003402:Creatine Kinase / Q000097:blood; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008297:Male; D017202:Myocardial Ischemia; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy*; D009206:Myocardium / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D015850:Interleukin-6; D016209:Interleukin-8; D014409:Tumor Necrosis Factor-alpha; D002392:Catechin; C045651:epigallocatechin gallate; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D003402:Creatine Kinase