Ischemia and
reperfusion injury (IRI) is a crucial contributor to the development of renal
fibrosis.
Ozone has been proposed as a novel medical
therapy for various conditions, including organ IRI. The aim of this study was to investigate whether
ozone oxidative preconditioning (OzoneOP) has a beneficial effect in preventing the development of renal
fibrosis following IRI. Sprague Dawley rats were subjected to 45 min of
ischemia followed by 8 weeks of reperfusion. Prior to surgery, rats in the OzoneOP group were treated with
ozone and those in the IRI and
Sham groups were untreated. Blood samples were collected for the detection of blood
urea nitrogen (BUN) and
creatinine (Cr) levels. To assess tissue
fibrosis, Masson's trichrome staining was performed. Immunohistochemistry was also performed to determine the localization of α-smooth muscle actin (α-SMA). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting were conducted to analyze the expression of
transforming growth factor (TGF)-β1, α-SMA and Smad7. The levels of BUN and Cr did not significantly differ between groups. Rats pretreated with
ozone showed markedly less interstitial
fibrosis than untreated rats following IRI. In addition, immunohistochemistry revealed that α-SMA expression was attenuated in the OzoneOP group compared with the IRI group. RT-qPCR and western blot analysis showed that OzoneOP inhibited the IRI-induced increases in α-SMA and TGF-β1 expression levels, and that the IRI-induced reduction in the expression of Smad7 was inhibited in the OzoneOP group. The results indicate that OzoneOP has beneficial effects on ischemic renal
fibrosis. OzoneOP may exert its protective effects by a mechanism involving modulation of the TGF-β1/Smad7 pathway.