Please use this identifier to cite or link to this item:
Full metadata record
DC FieldValueLanguage
dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP-
dc.contributor.authorSOUZA, Ana Carolina C. Pessoa de-
dc.contributor.authorVOLPINI, Rildo A.-
dc.contributor.authorSHIMIZU, Maria Heloisa-
dc.contributor.authorSANCHES, Talita Rojas-
dc.contributor.authorCAMARA, Niels Olsen Saraiva-
dc.contributor.authorSEMEDO, Patricia-
dc.contributor.authorRODRIGUES, Camila Eleuterio-
dc.contributor.authorSEGURO, Antonio Carlos-
dc.contributor.authorANDRADE, Lucia-
dc.identifier.citationAMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, v.302, n.8, p.F1045-F1054, 2012-
dc.description.abstractde Souza ACCP, Volpini RA, Shimizu MH, Sanches TR, Camara NOS, Semedo P, Rodrigues CE, Seguro AC, Andrade L. Erythropoietin prevents sepsis-related acute kidney injury in rats by inhibiting nuclear factor-kappa B and upregulating endothelial nitric oxide synthase. Am J Physiol Renal Physiol 302: F1045-F1054, 2012. First published January 11, 2012; doi:10.1152/ajprenal.00148.2011.-The pathophysiology of sepsis involves complex cytokine and inflammatory mediator networks, a mechanism to which NF-kappa B activation is central. Downregulation of endothelial nitric oxide synthase (eNOS) contributes to sepsis-induced endothelial dysfunction. Erythropoietin (EPO) has emerged as a major tissue-protective cytokine in the setting of stress. We investigated the role of EPO in sepsis-related acute kidney injury using a cecal ligation and puncture (CLP) model. Wistar rats were divided into three primary groups: control (sham-operated); CLP; and CLP + EPO. EPO (4,000 IU/kg body wt ip) was administered 24 and 1 h before CLP. Another group of rats received N-nitro-L-arginine methyl ester (L-NAME) simultaneously with EPO administration (CLP + EPO + L-NAME). A fifth group (CLP + EPOtreat) received EPO at 1 and 4 h after CLP. At 48 h postprocedure, CLP + EPO rats presented significantly higher inulin clearance than did CLP and CLP + EPO + L-NAME rats; hematocrit levels, mean arterial pressure, and metabolic balance remained unchanged in the CLP + EPO rats; and inulin clearance was significantly higher in CLP + EPOtreat rats than in CLP rats. At 48 h after CLP, creatinine clearance was significantly higher in the CLP + EPO rats than in the CLP rats. In renal tissue, pre-CLP EPO administration prevented the sepsis-induced increase in macrophage infiltration, as well as preserving eNOS expression, EPO receptor (EpoR) expression, IKK-alpha activation, NF-kappa B activation, and inflammatory cytokine levels, thereby increasing survival. We conclude that this protection, which appears to be dependent on EpoR activation and on eNOS expression, is attributable, in part, to inhibition of the inflammatory response via NF-kappa B downregulation.-
dc.description.sponsorshipBrazilian Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq, National Council for Scientific and Technological Development)-
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP, Foundation for the Support of Research in the State of Sao Paulo)-
dc.description.sponsorshipLaboratorios de Investigacao Medica, Medical Investigation Laboratories, Faculdade de Medicina da Universidade, Sao Paulo, University of Sao Paulo, School of Medicine, Hospital das Clinicas [FMUSP-HC/LIMs]-
dc.description.sponsorshipCNPq [141823/2007-0, 134318/2006-4, 309430/2006-7, 302835/2009-1]-
dc.description.sponsorshipFAPESP [06/56320-0]-
dc.relation.ispartofAmerican Journal of Physiology-Renal Physiology-
dc.subject.othercritically-ill patients-
dc.subject.otherseptic shock-
dc.titleErythropoietin prevents sepsis-related acute kidney injury in rats by inhibiting NF-kappa B and upregulating endothelial nitric oxide synthase-
dc.rights.holderCopyright AMER PHYSIOLOGICAL SOC-
dc.subject.wosUrology & Nephrology-
dc.type.categoryoriginal article-
dc.type.versionpublishedVersion-, Ana Carolina C. Pessoa de:Univ Sao Paulo, Dept Nephrol, Sch Med, BR-01246903 Sao Paulo, Brazil-, Niels Olsen Saraiva:Univ Sao Paulo, Dept Immunol, BR-01246903 Sao Paulo, Brazil; Univ Fed Sao Paulo, Dept Nephrol, Sao Paulo, Brazil-, Patricia:Univ Sao Paulo, Dept Immunol, BR-01246903 Sao Paulo, Brazil; Univ Fed Sao Paulo, Dept Nephrol, Sao Paulo, Brazil-
hcfmusp.relation.referenceAbdelrahman M, 2004, SHOCK, V22, P63, DOI 10.1097/01.shk.0000126869.21260.9d-
hcfmusp.relation.referenceANAGNOSTOU A, 1994, P NATL ACAD SCI USA, V91, P3974, DOI 10.1073/pnas.91.9.3974-
hcfmusp.relation.referenceAoshiba K, 2009, CRIT CARE MED, V37, P889, DOI 10.1097/CCM.0b013e31819b8371-
hcfmusp.relation.referenceBagnis C, 2001, NEPHROL DIAL TRANSPL, V16, P932, DOI 10.1093/ndt/16.5.932-
hcfmusp.relation.referenceBagshaw SM, 2007, CLIN J AM SOC NEPHRO, V2, P431, DOI 10.2215/CJN.03681106-
hcfmusp.relation.referenceBellomo R, 2008, NEPHRON EXP NEPHROL, V109, pE95, DOI 10.1159/000142933-
hcfmusp.relation.referenceBernhardt WM, 2008, CURR OPIN CRIT CARE, V14, P621, DOI 10.1097/MCC.0b013e328317ee82-
hcfmusp.relation.referenceBianca RDD, 2009, SHOCK, V31, P529, DOI 10.1097/SAK.0b013e31818909c0-
hcfmusp.relation.referenceBuras JA, 2005, NAT REV DRUG DISCOV, V4, P854, DOI 10.1038/nrd1854-
hcfmusp.relation.referenceCkless K, 2007, AM J RESP CELL MOL, V36, P645, DOI 10.1165/rcmb.2006-0329SM-
hcfmusp.relation.referenceCuzzocrea S, 2006, CRIT CARE MED, V34, P1168, DOI 10.1097/01.CCM.0000207346.56477.E8-
hcfmusp.relation.referenceDoi K, 2009, J AM SOC NEPHROL, V20, P1217, DOI 10.1681/ASN.2008060617-
hcfmusp.relation.referenceDoi K, 2009, J CLIN INVEST, V119, P2868, DOI 10.1172/JCI39421-
hcfmusp.relation.referenceDoi K, 2008, KIDNEY INT, V73, P1266, DOI 10.1038/ki.2008.97-
hcfmusp.relation.referencedu Cheyron D, 2005, INTENS CARE MED, V31, P1529, DOI 10.1007/s00134-005-2739-5-
hcfmusp.relation.referenced'Uscio LV, 2007, HYPERTENSION, V49, P1142, DOI 10.1161/HYPERTENSIONAHA.106.085704-
hcfmusp.relation.referenceEndre ZH, 2010, KIDNEY INT, V77, P1020, DOI 10.1038/ki.2010.25-
hcfmusp.relation.referenceFliser D, 2006, NAT CLIN PRACT CARD, V3, P563, DOI 10.1038/ncpcardio0609-
hcfmusp.relation.referenceFox AC, 2009, CRIT CARE MED, V37, P1138, DOI 10.1097/CCM.0b013e318196fd23-
hcfmusp.relation.referenceGilmore TD, 2006, ONCOGENE, V25, P6887, DOI 10.1038/sj.onc.1209982-
hcfmusp.relation.referenceHeeschen C, 2003, BLOOD, V102, P1340, DOI 10.1182/blood-2003-01-0223-
hcfmusp.relation.referenceHocherl K, 2010, AM J PHYSIOL-RENAL, V298, pF196, DOI 10.1152/ajprenal.90607.2008-
hcfmusp.relation.referenceHolly MK, 2006, KIDNEY INT, V70, P496, DOI 10.1038/
hcfmusp.relation.referenceHotchkiss RS, 2003, NEW ENGL J MED, V348, P138, DOI 10.1056/NEJMra021333-
hcfmusp.relation.referenceJansen TC, 2009, J TRAUMA, V66, P377, DOI [10.1097/TA.0b013e3181648e2f, 10.1097/TA.0b013e3l81648e2f]-
hcfmusp.relation.referenceJohnson DW, 2006, KIDNEY INT, V69, P1806, DOI 10.1038/
hcfmusp.relation.referenceKao R, 2007, CRIT CARE, V11, DOI 10.1186/cc5920-
hcfmusp.relation.referenceLacombe C, 1998, HAEMATOLOGICA, V83, P724-
hcfmusp.relation.referenceLeelahavanichkul A, 2008, AM J PHYSIOL-RENAL, V295, pF1825, DOI 10.1152/ajprenal.90442.2008-
hcfmusp.relation.referenceLiu SF, 2006, AM J PHYSIOL-LUNG C, V290, pL622, DOI 10.1152/ajplung.00477.2005-
hcfmusp.relation.referenceMEYER MH, 1985, ANAL BIOCHEM, V144, P285, DOI 10.1016/0003-2697(85)90118-6-
hcfmusp.relation.referenceMeyer-Schwesinger C, 2009, AM J PHYSIOL-RENAL, V296, pF1088, DOI 10.1152/ajprenal.90746.2008-
hcfmusp.relation.referenceMikkelsen ME, 2009, CRIT CARE MED, V37, P1670, DOI 10.1097/CCM.0b013e31819fcf68-
hcfmusp.relation.referenceMitra A, 2007, NEPHROL DIAL TRANSPL, V22, P2349, DOI 10.1093/ndt/gfm216-
hcfmusp.relation.referenceO'Sullivan AW, 2009, J SURG RES, V152, P46, DOI 10.1016/j.jss.2008.04.030-
hcfmusp.relation.referencePatel NSA, 2004, KIDNEY INT, V66, P983, DOI 10.1111/j.1523-1755.2004.00847.x-
hcfmusp.relation.referenceSanthanam AVR, 2005, STROKE, V36, P2731, DOI 10.1161/01.STR.0000190021.85035.5b-
hcfmusp.relation.referenceShang Y, 2009, CHINESE MED J-PEKING, V122, P834, DOI 10.3760/cma.j.issn.0366-6999.2009.07.014-
hcfmusp.relation.referenceSharples EJ, 2004, J AM SOC NEPHROL, V15, P2115, DOI 10.1097/01.ASN.0000135059.67385.5D-
hcfmusp.relation.referenceSHIH W, 1988, KIDNEY INT, V33, P1113, DOI 10.1038/ki.1988.119-
hcfmusp.relation.referenceSilver M, 2006, CRIT CARE MED, V34, P2310, DOI 10.1097/01.CCM.0000233873.17954.42-
hcfmusp.relation.referenceToth C, 2008, NEUROSCIENCE, V154, P767, DOI 10.1016/j.neuroscience.2008.03.052-
hcfmusp.relation.referencevan Doorn KJ, 2008, ACTA ANAESTH SCAND, V52, P1259, DOI 10.1111/j.1399-6576.2008.01738.x-
hcfmusp.relation.referenceVesey DA, 2004, NEPHROL DIAL TRANSPL, V19, P348, DOI 10.1093/ndt/gfg547-
hcfmusp.relation.referenceVILLA P, 1995, CLIN DIAGN LAB IMMUN, V2, P549-
hcfmusp.relation.referenceVolpini Rildo A., 2004, Nephron Physiology, V98, pP97, DOI 10.1159/000081558-
hcfmusp.relation.referenceWestenfelder C, 1999, KIDNEY INT, V55, P808, DOI 10.1046/j.1523-1755.1999.055003808.x-
hcfmusp.relation.referenceWICHTERMAN KA, 1980, J SURG RES, V29, P189, DOI 10.1016/0022-4804(80)90037-2-
hcfmusp.relation.referenceSharples EJ, 2006, NEPHRON EXP NEPHROL, V104, pE83, DOI 10.1159/000094546-
hcfmusp.relation.referenceYuen PST, 2004, AM J PHYSIOL-RENAL, V286, pF1116, DOI 10.1152/ajprenal.00366.2003-
hcfmusp.relation.referenceZhou M, 2007, MOL MED, V13, P488, DOI 10.2119/2007-00113.Zhou-
hcfmusp.relation.referenceZhou MA, 1997, BBA-GEN SUBJECTS, V1335, P182, DOI 10.1016/S0304-4165(96)00139-0-
Appears in Collections:

Artigos e Materiais de Revistas Científicas - FM/MCM
Departamento de Clínica Médica - FM/MCM

Artigos e Materiais de Revistas Científicas - HC/ICHC
Instituto Central - HC/ICHC

Artigos e Materiais de Revistas Científicas - LIM/12
LIM/12 - Laboratório de Pesquisa Básica em Doenças Renais

Files in This Item:
File Description SizeFormat 
  Restricted Access
publishedVersion (English)4.1 MBAdobe PDFView/Open Request a copy

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.