Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/58974
Type: Artigo de periódico
Title: p53-Mediated Oxidative Stress and Tubular Injury in Rats with Glycerol-Induced Acute Kidney Injury
Author: Homsi, E
da Silva, SM
de Brito, SM
Peixoto, EBI
de Faria, JBL
Janino, P
Abstract: Background/Aims: p53 is a transcriptional factor that responds to severe cell damage promoting the transcription of proapoptotic and prooxidant genes. In this study, we evaluated the role of p53 activation in glycerol-induced acute kidney injury (Gly-AKI). Methods: Rats were treated with p53 inhibitor (pifithrin-alpha) in the moment we injected glycerol. Renal function, renal histology (HE), TUNEL labeling, cleaved caspase-3 staining, renal p53, Bax, PUMA, Bcl-2, p21 and survivin expressions, renal lipid and DNA oxidative markers, and the expression of antioxidant enzymes (Mn-SOD, HO-1, and NAD(P)H:quinone-oxidoreductase-1) were evaluated. Results: Gly-AKI rats showed an increased renal expression of phosphorylated-p53. The p53 inhibitor attenuated renal impairment and significantly reduced tubular injury. The expression of the oxidative markers was significantly reduced in treated rats. Proapoptotic and prooxidant proteins Bax and PUMA were overexpressed in Gly-AKI rats and reduced in treated rats. On the contrary, antiapoptotic Bcl-2, p21, and survivin showed a tendency to increase in treated rats. The antioxidant enzymes' expression remained elevated or in-creased in treated rats. Conclusion: On the whole, p53 inhibition was protective in the short term. The oxidative stress subsided and the transcription tipped toward prosurvival genes; consequently tubular injury was attenuated in treated rats. Copyright (C) 2010 S. Karger AG, Basel
Subject: Acute kidney injury
Oxidative stress
Transcriptional factor
Apoptosis
p53
Country: Suíça
Editor: Karger
Rights: fechado
Identifier DOI: 10.1159/000322836
Date Issue: 2011
Appears in Collections:Unicamp - Artigos e Outros Documentos

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