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Protective Effects of Ozone Oxidative Postconditioning on Long-term Injury After Renal Ischemia/Reperfusion in Rat
Botao Jiang1, Yuqiang Su2, Qingzhi Chen3
1Center for Research and Technology of Precision Medicine, College of Life Sciences and Oceanography, Shenzhen University Xili Campus, Guangdong, People's Republic of China; Digestive Department, Second Affiliated Hospital of Xi'an Jiaotong University, Shaanxi, People's Republic of China.
Background:
Renal ischemia/reperfusion (I/R) injury can cause serious kidney damage (eg, acute aortic injury, chronic fibrosis). Some postconditioning treatments have been reported to protect from I/R effects. However, their mechanisms remain unclear. Here, we focused on potential protective effects of ozone on tubulointerstitial fibrosis after renal I/R injury in rats.
Methods:
Adult male rats were randomly divided into 4 groups with (1) sham-without I/R; (2) I/R-by clamping renal pedicle for 45 minutes; (3) I/R with ozone oxidative postconditioning (OzoneOP) following a 10-day reperfusion; and (4) I/R with oxygen oxidative postconditioning (OxygenOP) following a 10-day reperfusion. The kidneys were collected at 2 time points post I/R 10 days (at early phase) and 12 weeks (at late phase) and then analyzed for renal function, tissue fibrosis, and serum creatinine and urea nitrogen levels by staining and colorimetric methods. Additionally, expression levels of related fibrotic factors, such as α-smooth muscle actin, transforming growth factor β1, and phospho-Smad2, were assayed by immunochemistry staining.
Results:
OzoneOP treatment downregulated the α-smooth muscle actin, transforming growth factor β1, and phospho-Smad 2 protein expression in rats subjected to I/R at 10 days and 12 weeks. Moreover, it improved renal dysfunction and attenuated the patchy tubulointerstitial fibrosis.
Conclusion:
Ourdata indicate that I/R-induced renal damage might cause severe tubulointerstitial fibrosis at the late phase, and OzoneOP treatment may inhibit this fibrotic development.
