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Evaluation of the effects of a high dose of erythropoietin-beta on early endotoxemia using a rat model.

Authors: Eren, Z  Coban, J  Ekinci, ID  Kaspar, C  Kantarci, G 
Citation: Eren Z, etal., Adv Clin Exp Med. 2012 May-Jun;21(3):321-9.
Pubmed: (View Article at PubMed) PMID:23214195

BACKGROUND: Endotoxins can cause serious organ damage and death by triggering the secretion of pro-inflammatory cytokines such as TNF-alpha, IL-6 and IL-1beta in bacterial infections. OBJECTIVES: The goal of this study was to evaluate the effects of a high dose (3000 U/kg) of erythropoietin-beta (EPO) on inflammatory cytokine levels, renal function and histological changes during the early period of Lipopolysaccharide (LPS)-induced endotoxemia using a rat model. MATERIAL AND METHODS: Male Sprague Dawley (350-400 g) rats were randomized into 3 groups: Control group (n = 7); LPS group (received 20 mcg/kg LPS through intraperitoneal (i.p.) injection (n = 7); LPS+EPO group (received 3000 U/kg, ip 30 minutes before LPS administration (n = 7). Four hours after the administration of LPS, kidney tissue and serum samples were collected. Kidney function parameters, TNF-alpha, IL-6, IL-1beta, C reactive protein (CRP) and complete blood counts (CBC) were measured. The severity of renal tubular injury and caspase-9 immunoreactive cells was expressed as a percentage. RESULTS: Serum levels of urea, creatinine, TNF-alpha, IL-6 and IL-1beta were significantly increased in the LPS group (p < 0.0001 - p = 0.04) and were lower in LPS+EPO group (p < 0.0001, p = 0.01, p = 0.02, p = 01 and p < 0.0001, respectively). Pretreatment with EPO significantly increased platelet counts (p = 0.00) and decreased white blood cell counts (p = 0.02). The renal tubular injury percentage was significantly higher in the LPS group than in the control and LPS+EPO groups (p = 0.002, p = 0.003, and p = 0.005, respectively) and caspase-9 expression was lower in the LPS+EPO and control groups than in the LPS group. CONCLUSIONS: EPO might have renoprotective effects against the inflammatory process and cell apoptosis during endotoxemia.

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RGD Object Information
RGD ID: 10400903
Created: 2015-09-22
Species: All species
Last Modified: 2015-09-22
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.