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Eur J Pharmacol. 2012 Aug 15;689(1-3):154-9. doi: 10.1016/j.ejphar.2012.05.027. Epub 2012 May 30.

Erythropoietin attenuates cardiopulmonary bypass-induced renal inflammatory injury by inhibiting nuclear factor-κB p65 expression.

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1
Department of Cardiothoracic Surgery, Jinling Hospital, Clinical Medicine School of Nanjing University, 305 East Zhongshan Road, Nanjing 210002, China.

Abstract

Acute renal injury is one of the most frequent complications after cardiopulmonary bypass (CPB). This study was designed to evaluate the potential protective effect of erythropoietin (EPO) on CPB-induced renal injury in a rat model. Male Sprague-Dawley rats were randomly divided into three groups, sham-operated group (sham), control CPB group (control), erythropoietin CPB group (EPO). Blood samples were collected at the beginning, at the end of CPB, and at 0.5, 1, 2 and 24 h post-operation, and the kidneys were harvested 24 h postoperatively and observed by optical microscopy. Levels of serum creatinine (Cr) and blood urea nitrogen (BUN) were assayed. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6(IL-6) levels in the renal tissues were evaluated by the method of enzyme linked immunosorbent assay (ELISA). Protein and mRNA levels of nuclear factor kappa B p65 (NF-κB p65), intercellular adhesion molecule-1 (ICAM-1) were also determined using western blot and real-time PCR respectively. Serum Cr and BUN levels as well as TNF-α, IL-1β and IL-6 levels in renal tissues in control group were significantly higher than those in the sham group. However, the levels of above biomarkers were markedly decreased in EPO group when comparing with control group. Furthermore, NF-κB p65, ICAM-1 protein and mRNA expression were significantly down-regulated in EPO group comparing with control group. In addition, microscopic examinations revealed that histological injury was alleviated when treated with EPO. The results indicated that EPO potently protected against CPB-induced acute renal injury and inhibited expression of NF-κB p65 and inflammatory response.

PMID:
22659586
DOI:
10.1016/j.ejphar.2012.05.027
[Indexed for MEDLINE]

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