| Autor: |
Homsi, Eduardo, Mota da Silva, Jr., Sergio, Machado de Brito, Silvano, Bouçada Inácio Peixoto, Elisa, Butori Lopes de Faria, Jose, Janino, Patrícia, Mota da Silva, Sergio Jr, Bouçada Inácio Peixoto, Elisa, Janino, Patrícia |
| Zdroj: |
American Journal of Nephrology; 2011, Vol. 33 Issue 1, p49-59, 11p, 8 Graphs |
| Abstrakt: |
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-α) 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 increased 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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