Transplantation Proceedings
Volume 41, Issue 9 , Pages 3585-3589, November 2009

Down-Regulation of Cyclooxygenase-2 is Involved in Ischemic Postconditioning Protection Against Renal Ischemia Reperfusion Injury in Rats

  • Y. Yun

      Affiliations

    • Faculty of Pharmacy and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming P.R. China
    • Department of Pharmacology, Kunming Medical College, Kunming P.R. China
    • ,
  • W.G. Duan

      Affiliations

    • Key Laboratory of Molecular Biology for Sinomedicine, Yunnan University of Traditional Chinese Medicine, Kunming P.R. China
    • ,
  • P. Chen

      Affiliations

    • Faculty of Pharmacy and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming P.R. China
    • ,
  • H.X. Wu

      Affiliations

    • Faculty of Pharmacy and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming P.R. China
    • ,
  • Z.Q. Shen

      Affiliations

    • Faculty of Pharmacy and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming P.R. China
    • ,
  • Z.Y. Qian

      Affiliations

    • Faculty of Pharmacy and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming P.R. China
    • ,
  • D.H. Wang

      Affiliations

    • Faculty of Pharmacy and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming P.R. China
    • Corresponding Author InformationAddress reprint requests to Dian Hua Wang, Faculty of Pharmacy and Yunnan Laboratory for Natural Products, Kunming Medical College, 191 Western People's Road, Kunming 650031, P.R. China

Abstract 

Ischemic postconditioning (IPostC) is a phenomenon whereby rapid intermittent interruptions of blood flow in the early phase of reperfusion protect an organ from ischemia-reperfusion injury. In the present study, we investigated whether the protective effect of IPostC was associated with the cyclooxygenase-2 (COX-2) pathway by evaluating its expression following renal ischemia-reperfusion in rats. Animals underwent 45 minutes of renal pedicle occlusion followed by reperfusion for 1.5, 3, 6, 12, or 24 hours. IPostC was performed by six 10-second cycles of reperfusion and 10 seconds of renal pedicle occlusion at the end of ischemia. Blood and kidney samples were collected at each reperfusion time point. The protein expression of COX-1 and COX-2 were evaluated by Western blotting. Our data showed that IPostC attenuated the renal dysfunction and decreased COX-2 expression induced by ischemia-reperfusion insults. The results indicated that the protective effect of IPostC was related to down-regulation of COX-2 expression.

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 The study was partially supported by a grant (11415018) from the Department of Graduate, Kunming Medical College of China.

PII: S0041-1345(09)01379-7

doi:10.1016/j.transproceed.2009.06.209

Transplantation Proceedings
Volume 41, Issue 9 , Pages 3585-3589, November 2009

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