Erythropoietin attenuates renal injury in experimental acute renal failure ischaemic/reperfusion model

Spandou, Evangelia; Tsouchnikas, Ioannis; Karkavelas, George; Dounousi, Evangelia; Simeonidou, Constantina; Guiba-Tziampiri, Olympia; Tsakiris, Dimitrios

doi:10.1093/ndt/gfi177

Cited by 156 publications

(120 citation statements)

References 17 publications

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“…Also apoptotic markers like BAX were reduced and the TUNEL assay showed only some positive cells. 9 This effect of renal tissue protection by EPO application was also seen in other rodent models. [10][11][12] Not only small animal models, but also experimental set-up with large animals that are much closer to clinical reality showed these positive effects.…”

supporting

confidence: 52%

Kidney Ischemia and Reperfusion Injury – Field of Glory or Warterloo for Erythropoietin?

Simon¹,

Schelzig²,

Oberhuber³

2016

Nephrol Open J

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supporting

confidence: 52%

Kidney Ischemia and Reperfusion Injury – Field of Glory or Warterloo for Erythropoietin?

Simon¹,

Schelzig²,

Oberhuber³

2016

Nephrol Open J

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“…A number of clinical and experimental studies have demonstrated that NF-κB, a transcription factor, plays a central role in renal pathology (6). Spandou et al reported that renal I/R leads to the activation of NF-κB, which suggests that it may be a marker of injury linked to the pathophysiology of a variety of renal disorders, including I/R, and that its inhibition prevents in vivo cell apoptosis associated with renal I/R injury (20). Therefore, inhibition of the permanent activation of NF-κB protects renal tissue from ischemic injury.…”

Section: Discussionmentioning

confidence: 99%

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

Kinaci

Erkasap

Küçük

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. The aim of this study was to investigate the effects of quercetin on nitric oxide synthase (NOS), nuclear factor-κB (NF-κB) and apoptosis in renal ischemia/reperfusion (I/R) injury in rats. A total of 42 Sprague-Dawley rats were divided into three groups. The control, I/R and I/R+quercetin (I/R+Q) groups were treated with quercetin (50 mg/kg intraperitoneal) 1 h prior to the induction of ischemia. Tissue malondialdehyde (MDA) and glutathione (GSH) levels were determined by high-performance liquid chromatography (HPLC). p53, endothelial NOS (eNOS) and NF-κB expression were assessed immunohistochemically, and apoptosis assesment was performed using terminal deoxy nucleotidyl transferase dUTP nick end-labeling (TUNEL) assay. The mRNA levels of inducible NOS (iNOS) in renal tissue were determined by realtime polymerase chain reaction (RT-PCR). MDA levels were significantly decreased in the quercetin group compared to the I/R group. However, GSH levels were significantly increased with quercetin treatment in the I/R group. Histological results, the number of apoptotic and p53-positive cells, NF-κB and eNOS expression levels were significantly decreased in the quercetin treatment group compared to the I/R group. iNOS gene expression increased in the I/R group, but no significant difference was found between the I/R and quercetin treatment groups. Therefore, quercetin not only has antioxidant and antiapoptotic activities, but also has an inhibitory effect on eNOS and NF-κB for renal tissue protection during I/R injury in rats. Therefore, quercetin may be a promising renoprotective therapeutic agent.

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“…Akt can significantly increase NF-κB and HIF-1 activation resulting in the enhancement of EPO expression. Although in instances that involve some EPO receptorpositive tumors or specific ischemia-reperfusion cardiac injury models, EPO under most conditions uses NF-κB to prevent apoptosis through the enhanced expression and translocation of NF-κB to the nucleus to elicit anti-apoptotic gene activation [25,27,64].…”

Section: Wnt Gsk-3β Nf-κb and Epomentioning

confidence: 99%

Raves and risks for erythropoietin

Maiese

Chong²,

Shang³

2008

Cytokine & Growth Factor Reviews

125

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Global use of erythropoietin (EPO) continues to increase as a proven agent for the treatment of anemia. Yet, EPO is no longer believed to have exclusive biological activity in the hematopoietic system and is now considered applicable for a variety of disorders such as diabetes, Alzheimer's disease, and cardiovascular disease. Treatment with EPO is considered to be robust and can prevent metabolic compromise, neuronal and vascular degeneration, and inflammatory cell activation. On the converse side, observations that EPO administration is not without risk have fueled controversy. Here we present recent advances that have elucidated a number of novel cellular pathways governed by EPO to open new therapeutic avenues for this agent and avert its potential deleterious effects. Keywordsangiogenesis; cardiac; diabetes; erythropoietin; neurodegeneration Historical Background for ErythropoietinInitially termed "hemopoietine", erythropoietin (EPO) became evident as a factor that could stimulate new red blood cell development through the pioneering studies of Carnot and Deflandre in 1906 [1]. This team of investigators demonstrated that plasma removed from rabbits following a bleeding stimulus that was later injected into control untreated rabbits would lead to the development of immature red blood cells, or reticulocytosis. A number of other investigators followed these studies that demonstrated similar findings that plasma from animals that were bled would yield a significant reticulocytosis. Interestingly, more elegant experiments later demonstrated that a rise in hemoglobin levels with reticulocytosis occurred in parabiotic rats when only one partner was exposed to hypoxia, illustrating that depressed oxygen tensions could stimulate EPO production. Eventually, human EPO protein was purified that paved the way for the cloning of the EPO gene and the development of recombinant EPO for clinical use [2,3]. *Corresponding Author: Kenneth Maiese, MD, Department of Neurology, 8C-1 UHC, Wayne State University School of Medicine, 4201 St. Antoine, Detroit,; email: aa2088@wayne.edu, kmaiese@med.wayne.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. The production and secretion of the mature EPO also relies upon the integrity of the N-and O-linked chains. The EPO gene is located on chromosome 7, exists as a single copy in a 5.4 kb region of the genomic DNA, and encodes a polypeptide chain containing 193 amino acids. During the production and secretion of EPO, a 166 amino acid peptide is initially generated following the cleavage of a 27 amino acid hydrophobic secretory leader ...

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Erythropoietin attenuates renal injury in experimental acute renal failure ischaemic/reperfusion model

Cited by 156 publications

References 17 publications

Kidney Ischemia and Reperfusion Injury – Field of Glory or Warterloo for Erythropoietin?

Kidney Ischemia and Reperfusion Injury – Field of Glory or Warterloo for Erythropoietin?

Effects of quercetin on apoptosis, NF-κB and NOS gene expression in renal ischemia/reperfusion injury

Raves and risks for erythropoietin

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