Silymarin exacerbates p53-mediated tubular apoptosis in glycerol-induced acute kidney injury in rats

dc.creatorHomsi, E
dc.creatorde Brito, SM
dc.creatorJanino, P
dc.date2010
dc.date2014-11-14T05:59:23Z
dc.date2015-11-26T16:04:45Z
dc.date2014-11-14T05:59:23Z
dc.date2015-11-26T16:04:45Z
dc.date.accessioned2018-03-28T22:53:53Z
dc.date.available2018-03-28T22:53:53Z
dc.identifierRenal Failure. Informa Healthcare, v. 32, n. 5, n. 623, n. 632, 2010.
dc.identifier0886-022X
dc.identifierWOS:000283115300014
dc.identifier10.3109/08860221003778064
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/75604
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/75604
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/75604
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1265566
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionBackground/aims: Silymarin is an herbal extract with antioxidant properties that can reduce oxidative stress-mediated injuries in murine models of liver, heart, and kidney diseases. Silymarin can also increase p53-mediated cellular apoptosis in vitro. We tested the effect of silymarin administration before glycerol-induced acute kidney injury (Gly-AKI) in rats. Methods: Renal function, tubular injury, oxidative stress, leukocytes infiltration, and renal expression of apoptosis regulating proteins (p53, p-p53, Bax, Bcl-2, survivin, and cleaved caspase-3) were evaluated 6 or 24 h after glycerol. Results: Silymarin exacerbated the renal impairment and tubular apoptosis but had no effect on tubular necrosis or renal leukocytes infiltration. Renal lipid and DNA peroxidation was increased after glycerol and silymarin did not reduce oxidative stress. Proteins p53, p-p53, and proapoptotic Bax were upregulated in Gly-AKI rats treated with silymarin, whereas anti-apoptotic Bcl-2 was reduced in this group. Cleaved caspase-3 was overexpressed in Gly-AKI rats, particularly when treated with silymarin. Survivin was less expressed in Gly-AKI than in controls, but this deficit was not aggravated by silymarin. Conclusion: The persistence of oxidative stress, inflammatory reaction, and tubular necrosis, as well as exacerbation of p53-mediated tubular apoptosis, led to a more severe renal impairment in Gly-AKI rats treated with silymarin.
dc.description32
dc.description5
dc.description623
dc.description632
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageen
dc.publisherInforma Healthcare
dc.publisherLondon
dc.publisherInglaterra
dc.relationRenal Failure
dc.relationRen. Fail.
dc.rightsfechado
dc.rightshttp://informahealthcare.com/userimages/ContentEditor/1255620309227/Copyright_And_Permissions.pdf
dc.sourceWeb of Science
dc.subjectacute kidney injury
dc.subjectsilymarin
dc.subjectantioxidant
dc.subjectapoptosis
dc.subjectp53
dc.subjectcaspase-3
dc.subjectsurvivin
dc.subjectAcute-renal-failure
dc.subjectInduced Oxidative Stress
dc.subjectWild-type P53
dc.subjectNf-kappa-b
dc.subjectCell-cycle
dc.subjectP53-induced Apoptosis
dc.subjectSilibinin Protects
dc.subjectInduced Activation
dc.subjectGene-expression
dc.subjectDown-regulation
dc.titleSilymarin exacerbates p53-mediated tubular apoptosis in glycerol-induced acute kidney injury in rats
dc.typeArtículos de revistas


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