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Journals Molecular and Cellular Biochemistry Volume 346 Issue 1

Chuanjun Zhuo Ying Wang Xiaohui Wang Yufen Wang Yuhui Chen +86-22-24390963 +86-22-24390963 chenyuhuitj@yahoo.com.cn Department of Psychiatry Anning Hospital of Tianjin City No. 20 Yongping Lane, Dongli District Tianjin 300300 China Department of Psychiatry the 261st Hospital of Chinese People’s Liberation Army Haidian District Beijing 100094 China Abstract Ischemic postconditioning (IPC) represents one of the most effective cardioprotective strategies against myocardial ischemia/reperfusion. Depression is commonly present in patients with coronary heart disease. However, whether depression interferes with the cardioprotection of IPC during myocardial ischemia/reperfusion and their underlying mechanisms remain largely unknown. Isolated hearts from chronic mild stress induced-depressed rats and non-depressed rats were subjected to 30 min of regional ischemia followed by 120 min of reperfusion in the presence or absence of IPC (consisting of 6 cycles of 10 s of reperfusion and 10 s of ischemia immediately after the sustained ischemia). Myocardial infarct size, creatine kinase (CK) and cardiac troponin T (cTnT) release, cardiac function and phosphorylated AKT and signal transducer and activator of transcription-3 (STAT-3) were measured. IPC significantly prevented the hearts from myocardial ischemia/reperfusion injury by decreasing infarct size, and CK and cTnT release in coronary effluent, and improving cardiac functional recovery in non-depressed rats. However, these cardioprotective effects of IPC were not observed in depressed rats. In addition, IPC had no effects on the phosphorylation of AKT and STAT-3 at reperfusion in depressed hearts, although it markedly increased the phosphorylation of AKT and STAT-3 at reperfusion in non-depressed hearts. In conclusion, these data indicate that cardioprotection by IPC is abolished during myocardial ischemia/reperfusion in depressed rats, and the underlying mechanisms are probably related to the impaired activation of AKT and STAT-3 at reperfusion.

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Cardioprotection by ischemic postconditioning is abolished in depressed rats: role of Akt and signal transducer and activator of transcription-3

More Info
  • Publisher Springer US
  • Copyright Copyright © 2011 by Springer Science+Business Media, LLC.
  • Subject Life Sciences; Cardiology; Oncology; Medical Biochemistry; Biochemistry, general
  • ISSN 0300-8177
  • eISSN 1573-4919
  • D.O.I. 10.1007/s11010-010-0589-0
  • Publisher site Get PDF  

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