Hypercholesterolemia Abrogates the Cardioprotection of Ischemic Postconditioning in Isolated Rat Heart: Roles of Glycogen Synthase Kinase-3β and the Mitochondrial Permeability Transition Pore

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• 作者：Nan Wu (1)
  Xiaowen Zhang (2)
  Yuee Guan (1)
  Wenqi Shu (1)
  Pengyu Jia (3)
  Dalin Jia (1)
  
• 关键词：Ischemic postconditioning ; Hypercholesterolemia ; Glycogen synthase kinase ; 3β ; Mitochondrial permeability transition pore
• 刊名：Cell Biochemistry and Biophysics
• 出版年：2014
• 出版时间：May 2014
• 年：2014
• 卷：69
• 期：1
• 页码：123-130
• 全文大小：595 KB
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• 作者单位：Nan Wu (1)
  Xiaowen Zhang (2)
  Yuee Guan (1)
  Wenqi Shu (1)
  Pengyu Jia (3)
  Dalin Jia (1)
  
  1. Department of Cardiology, The First Affiliated Hospital of China Medical University, 155th North of Nanjing Street, Heping District, Shenyang, 110001, Liaoning, China
  2. Department of Medical Genetics, China Medical University, Shenyang, Liaoning, China
  3. China Medical University, Shenyang, Liaoning, China
  
• ISSN：1559-0283

文摘

Ischemic postconditioning (IPO) reduces lethal reperfusion injury under normal conditions, but its effectiveness in hypercholesterolemia (HC) is disputed. We measured the cardioprotection of IPO in hypercholesterolemic rats and determined the roles of glycogen synthase kinase-3β (GSK-3β) and the mitochondrial permeability transition pore (mPTP). Isolated rat hearts underwent 30-min global ischemia and 120-min reperfusion. Postconditioning protocol induced six cycles of 10s ischemia and 10s reperfusion at the onset of the reperfusion. Myocardial infarct size was estimated by triphenyltetrazolium chloride staining and cardiomyocyte apoptosis was assessed by TUNEL staining. GSK-3β phosphorylation was measured by immunoblotting. The opening of mPTP was measured by NAD+ content in myocardium. In normocholesterolemia (NC) groups, infarct size and cardiomyocyte apoptosis were significantly reduced after IPO. These reductions were completely abolished by HC, as evidenced by a similar infarct size and cardiomyocyte apoptosis observed between the IPO-HC and IR (ischemia–reperfusion)-HC groups. GSK-3β phosphorylation was significantly higher in the IPO-NC than the IPO-HC group. In addition, NAD+ content in myocardium, a marker of mPTP opening, was higher in the IPO-NC group than the IPO-HC group. In conclusion, cardioprotection of IPO is blocked by hypercholesterolemia. This might be due to the impairment of phosphorylation of GSK-3β and attenuation of mPTP opening.