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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorZAMBOM, Fernanda Florencia Fregnan
dc.contributor.authorOLIVEIRA, Karin Carneiro
dc.contributor.authorFORESTO-NETO, Orestes
dc.contributor.authorFAUSTINO, Viviane Dias
dc.contributor.authorAVILA, Victor Ferreira
dc.contributor.authorALBINO, Amanda Helen
dc.contributor.authorARIAS, Simone Costa Alarcon
dc.contributor.authorVOLPINI, Rildo Aparecido
dc.contributor.authorMALHEIROS, Denise Maria Avancini Costa
dc.contributor.authorCAMARA, Niels Olsen Saraiva
dc.contributor.authorZATZ, Roberto
dc.contributor.authorFUJIHARA, Clarke Kazue
dc.date.accessioned2019-11-06T18:50:11Z-
dc.date.available2019-11-06T18:50:11Z-
dc.date.issued2019
dc.identifier.citationAMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, v.317, n.4, p.F1058-F1067, 2019
dc.identifier.issn1931-857X
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/34097-
dc.description.abstractNitric oxide inhibition with N-omega-nitro-L-arginine methyl ester (L-NAME), along with salt overload, leads to hypertension, albuminuria, glomerulosclerosis, glomerular ischemia, and interstitial fibrosis, characterizing a chronic kidney disease (CKD) model. Previous findings of this laboratory and elsewhere have suggested that activation of at least two pathways of innate immunity, Toll-like receptor 4 (TLR4)/NF-kappa B and nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain containing 3 (NLRP3) inflammasome/IL-1 beta, occurs in several experimental models of CKD and that progression of renal injury can be slowed with inhibition of these pathways. In the present study, we investigated whether activation of innate immunity, through either the TLR4/NF-kappa B or NLRP3/IL-1 beta pathway, is involved in the pathogenesis of renal injury in chronic nitric oxide inhibition with the salt-overload model. Adult male Munich-Wistar rats that received L-NAME in drinking water with salt overload (HS + N group) were treated with allopurinol (ALLO) as an NLRP3 inhibitor (HS + N + ALLO group) or pyrrolidine dithiocarbamate (PDTC) as an NF-kappa B inhibitor (HS + N + PDTC group). After 4 wk, HS + N rats developed hypertension, albuminuria, and renal injury along with renal inflammation, oxidative stress, and activation of both the NLRP3/IL-1 beta and TLR4/NF-kappa B pathways. ALLO lowered renal uric acid and inhibited the NLRP3 pathway. These effects were associated with amelioration of hypertension, albuminuria, and interstitial inflammation/fibrosis but not glomerular injury. PDTC inhibited the renal NF-kappa B system and lowered the number of interstitial cells staining positively for NLRP3. PDTC also reduced renal xanthine oxidase activity and uric acid. Overall, PDTC promoted a more efficient anti-inflammatory and nephroprotective effect than ALLO. The NLRP3/IL-1 beta and TLR4/NF-kappa B pathways act in parallel to promote renal injury/inflammation and must be simultaneously inhibited for best nephroprotection.eng
dc.description.sponsorshipSao Paulo Research Foundation (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo) [2012/10926-5, 2015/25368-6]
dc.description.sponsorshipNational Council for Scientific and Technological Development Award [303684/2013-5]
dc.language.isoeng
dc.publisherAMER PHYSIOLOGICAL SOCeng
dc.relation.ispartofAmerican Journal of Physiology-Renal Physiology
dc.rightsrestrictedAccesseng
dc.subjectchronic kidney diseaseeng
dc.subjecthigh salteng
dc.subjecthypertensioneng
dc.subjectinflammationeng
dc.subjectinnate immunityeng
dc.subjectnitric oxideeng
dc.subject.othernf-kappa-beng
dc.subject.othervascular smooth-muscleeng
dc.subject.othernitric-oxide synthesiseng
dc.subject.othernlrp3 inflammasome activationeng
dc.subject.othercortical tubulointerstitial injuryeng
dc.subject.otherblood-pressureeng
dc.subject.otherrenal injuryeng
dc.subject.otheruric-acideng
dc.subject.otheroxidative stresseng
dc.subject.othercellseng
dc.titlePathogenic role of innate immunity in a model of chronic NO inhibition associated with salt overloadeng
dc.typearticleeng
dc.rights.holderCopyright AMER PHYSIOLOGICAL SOCeng
dc.identifier.doi10.1152/ajprenal.00251.2019
dc.identifier.pmid31411073
dc.subject.wosPhysiologyeng
dc.subject.wosUrology & Nephrologyeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
hcfmusp.description.beginpageF1058
hcfmusp.description.endpageF1067
hcfmusp.description.issue4
hcfmusp.description.volume317
hcfmusp.origemWOS
hcfmusp.origem.idWOS:000489947900028
hcfmusp.origem.id2-s2.0-85073082684
hcfmusp.publisher.cityBETHESDAeng
hcfmusp.publisher.countryUSAeng
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dc.description.indexMEDLINEeng
dc.identifier.eissn1522-1466
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