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.
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.
Authors: Tao Qiu; Zhi-Shun Wang; Xiu-Heng Liu; Hui Chen; Jiang-Qiao Zhou; Zhi-Yuan Chen; Min Wang; Guan-Jun Jiang; Lei Wang; Gang Yu; Long Zhang; Ye Shen; Lu Zhang; Li He; Hua-Xin Wang; Wen-Jing Zhang Journal: Exp Ther Med Date: 2017-03-08 Impact factor: 2.447
Authors: Boris Betz; Reinhard Schneider; Tobias Kress; Martin Alexander Schick; Christoph Wanner; Christoph Sauvant Journal: PPAR Res Date: 2012-02-15 Impact factor: 4.964
Authors: C Di Filippo; M C Trotta; R Maisto; D Siniscalco; M Luongo; L Mascolo; R Alfano; M Accardo; C Rossi; F Ferraraccio; M D'Amico Journal: Oxid Med Cell Longev Date: 2015-07-21 Impact factor: 6.543