Ischemic postconditioning attenuates inflammation in rats following renal ischemia and reperfusion injury.

Ischemic postconditioning (IPoC) involves a series of brief rapid intermittent ischemic episodes applied at the onset of reperfusion in the previously ischemic tissue or organ. Previous studies have demonstrated that IPoC attenuates tissue damage induced by ischemia and reperfusion (I/R) injury. The aim of the present study was to investigate whether IPoC has a beneficial effect on inflammation in a rat model of renal I/R injury. Wistar rats were subjected to 45 min of ischemia followed by 24, 72 or 120 h of reperfusion (I/R group). In the IPoC group, rats subjected to I/R were treated with six cycles of 10 sec reperfusion followed by a 10-sec ischemic episode. Blood samples were collected for the determination of blood urea nitrogen (BUN) and creatinine (Cr) levels. Furthermore, histological examination and immunohistochemical staining for the localization of nuclear factor-κB (NF-κB) were performed. In addition, quantitative polymerase chain reaction (qPCR) analysis was used to determine the expression levels of intercellular adhesion molecule-1 (ICAM-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), while western blot analysis was used to detect the protein expression levels of NF-κB. The results indicated that the BUN and Cr levels increased significantly in the I/R group, while the IPoC rats showed evidently reduced renal damage. Immunohistochemical analysis revealed that the expression levels of NF-κB were decreased by IPoC. In addition, the qPCR results revealed that IPoC significantly inhibited the increased mRNA expression levels of ICAM-1, IL-6 and TNF-α, induced by I/R injury. Western blot analysis indicated that the expression levels of NF-κB were upregulated in the I/R group, while IPoC was shown to inhibit the expression. In conclusion, IPoC was demonstrated to exhibit potent anti-inflammatory properties against renal I/R injury.