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• W2018798974 abstract "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. 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. 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. 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. 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." @default.
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• W2018798974 date "2008-10-01" @default.
• W2018798974 modified "2023-09-27" @default.
• W2018798974 title "Ozone Oxidative Preconditioning Protects the Rat Kidney from Reperfusion Injury: The Role of Nitric Oxide" @default.
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• W2018798974 doi "https://doi.org/10.1016/j.jss.2007.12.756" @default.
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