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J Surg Res. 2014 Jan;186(1):398-407. doi: 10.1016/j.jss.2013.07.048. Epub 2013 Aug 13.

Celastrol protects kidney against ischemia-reperfusion-induced injury in rats.

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  • 1Department of Urology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.



Ischemia-reperfusion (IR) causes various damages in renal tissues, which is exacerbated by hypoxia-induced excessive inflammation and deteriorates the prognosis of patients after kidney surgery. Celastrol is a potent inflammation inhibitor that has little toxicity. In this report, we investigated whether celastrol protects against IR-induced renal injury in rats.


Renal IR injury was induced by occlusion of the bilateral renal pedicles for 45 min followed by reperfusion for 6 h. Celastrol or vehicle solution was intraperitoneally injected 30 min before renal ischemia, respectively. Renal histology, function, and pro-inflammatory cytokines and mediators were assessed. The effect of celastrol on nuclear translocation of nuclear factor kappa B (NF-κB) was also measured.


Celastrol significantly suppressed elevation of the renal function markers and the lipid peroxidation level, alleviated renal tubular damage, and decreased the levels of tumor necrosis factor-α, interleukin-1β, and monocyte chemotactic protein-1 (MCP-1) messenger RNA in kidney caused by IR. Moreover, celastrol prevented IR-induced expression of pro-inflammatory mediators, which was associated with suppression of nuclear translocation of NF-κB subunit p65.


Celastrol ameliorated the acute kidney injury caused by IR, which was associated with inhibiting local NF-κB activation and inflammation. Our findings suggest that celastrol could be useful for preventing IR-induced renal injury.

Copyright © 2014 Elsevier Inc. All rights reserved.


Celastrol; Inflammation; NF-κB; Renal ischemia–reperfusion

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