Ischemic postconditioning inhibits the renal fibrosis induced by ischemia-reperfusion injury in rats

Urology
Xiaodong WengHui Chen

Abstract

To investigate whether ischemic postconditioning effects on the development of tubulointerstitial fibrosis follow acute renal ischemia-reperfusion. Rat models of warm renal I/R were established by clamping left pedicles for 45 minutes after right nephrectomy, both with and without treatment with ischemic postconditioning, and then reperfused for up to 12 weeks. Hematoxylin-eosin (H&E) and Masson's trichrome staining were used to assess renal fibrosis. The expression spot and protein levels of α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), and phospho-Smad2 were also analyzed. Our data showed that patchy inflammation and tubulointerstitial fibrosis were found 12 weeks later in rats subjected to I/R alone or with postconditioning. Tubulointerstitial fibrosis worsened further in rats subjected to 45-minute ischemia-reperfusion, accompanied by the increased expressions of α-SMA, TGF-β1, and phospho-Smad2 at the end of 12 weeks. In contrast, the above histologic changes and molecular expressions were significantly attenuated in rats of ischemic postconditioning group. The results indicated that 45-minute I/R injury may cause tubulointerstitial fibrosis in the long term, and ischemic postconditioning has benef...Continue Reading

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Citations

Aug 27, 2014·Renal Failure·Hui ChenXiuheng Liu
Mar 23, 2013·Transplantation·Eline K van den AkkerFrank J M F Dor
Nov 6, 2014·Experimental and Therapeutic Medicine·Lei WangHeng-Cheng Zhu
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Oct 9, 2013·Transplantation·Eline K van den AkkerFrank J M F Dor

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