Journal of Surgical Research
Volume 149, Issue 2 , Pages 287-295, October 2008

Ozone Oxidative Preconditioning Protects the Rat Kidney from Reperfusion Injury: The Role of Nitric Oxide

  • Hui Chen, M.D.

      Affiliations

    • Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China
  • ,
  • Bianzhi Xing, M.D.

      Affiliations

    • Department of Neurology, Tongji Hospital, Tongji Medical College, HUST, Wuhan, China
  • ,
  • Xiuheng Liu, Ph.D.

      Affiliations

    • Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China
    • Corresponding Author InformationTo whom correspondence and reprint requests should be addressed at Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Jiefang Road 238, Wuhan, 430060, China
  • ,
  • Bingyan Zhan, M.D.

      Affiliations

    • Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China
  • ,
  • Jiangqiao Zhou, M.D.

      Affiliations

    • Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China
  • ,
  • Hengcheng Zhu, M.D.

      Affiliations

    • Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China
  • ,
  • Zhiyuan Chen, M.D.

      Affiliations

    • Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China

Received 25 July 2007 published online 13 February 2008.

Background

Ischemia/reperfusion (I/R) injury, which is commonly seen in the field of renal surgery or transplantation, is a major cause of acute renal failure. Previous studies have shown that ozone oxidative preconditioning (OzoneOP) attenuated renal I/R injury. The objective of this study was to examine the hypothesis that protective effects of OzoneOP in renal I/R injury were associated with endogenous NO.

Materials and methods

In a right-nephrectomized rat mode, anesthetized rats underwent 45 min of renal ischemia. OzoneOP (1 mg/kg) was administered before I/R injury. Rats were killed at 24, 48, and 72 h after I/R injury and blood samples and renal tissues were obtained.

Results

OzoneOP prevented the renal dysfunction induced by I/R and increased nitric oxide (NO) release and renal NO synthase (endothelial, eNOS, and inducible, iNOS) expression. In contrast, enhancement of endothelin-1 in the kidney after the reperfusion was markedly suppressed by OzoneOP.

Conclusions

Our findings indicated that the protective effect of OzoneOP was closely related to the NO production following the increase in eNOS and iNOS expression. Ozone treatment may have important clinical implications, particularly in view of the minimizing renal damage before transplantation.

Key Words: ozone oxidative preconditioning, ischemia/reperfusion, NO, eNOS, iNOS, ET-1

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PII: S0022-4804(07)02408-0

doi:10.1016/j.jss.2007.12.756

Journal of Surgical Research
Volume 149, Issue 2 , Pages 287-295, October 2008