Evaluation of the effects of a high dose of erythropoietin-beta on early endotoxemia using a rat model
Eren, Z. | Çoban, J. | Ekinci, I.D. | Kaspar, C. | Kantarci, G.
Article | 2012 | Advances in Clinical and Experimental Medicine21 ( 3 ) , pp.321 - 329
Background. Endotoxins can cause serious organ damage and death by triggering the secretion of pro-inflammatory cytokines such as TNF-?, IL-6 and IL-Iß 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.) in . . .jection (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-?, IL-6, IL-1ß, 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-?, IL-6 and IL-1ß 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. © Copyright by Wroclaw Medical University
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