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IL-37b protects against renal ischemic/reperfusion injury via inhibition NF-kB up-regulation

 
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Research Article 
dx.doi.org/10.18081/2333-5106/016-2/25-32
American Journal of BioMedicine Volume 4, Issue 1, pages 25-32
Received November 22, 2015; accepted January 29, 2016; published February 23, 2016 

 Yan Xina, b, Howard D. Kirshnera, c, Carmen A. Peraltaa, Richard A. Ciavarraamail of corresponding author

Abstract

IL-37 member suppresses inflammation among the various splicing forms of IL-37, IL-37b with unclear signaling pathway. Acute kidney injury resulted from ischemia and reperfusion is a significant clinical problem in cardiovascular medical and surgical procedures. In this study, we investigated the effects of IL-37b renal I/R injury in mice and to determine the involvement of nuclear factor kappa B (NF-kB) activation in the effects. Renal I/R was induced by right renal pedicle clamping for 45 min and left nephrectomy. Sham-operated mice with no occlusion of the renal vessel. I/R mice received an injection of recombinant IL-37b or vehicle, immediately before reperfusion. Compared with vehicle treatment, mice treated with recombinant IL-37b attenuates I/R-induced TNFα, IL-1β, and IL-6, inhibited the up-regulation of NF-kB activation after I/R with decreased the levels of plasma of both creatinine and urea. In conclusion; IL-37b exerts effects in vivo by modulating the NF-kB activation.

Keywords: IL37; Renal I/R; Cardiovascular diseases; Recombinant IL-37b

Copyright © 2016 by The American Society for BioMedicine and BM-Publisher, Inc.

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