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Utilize este identificador para citar ou criar um link para este item: http://acervodigital.unesp.br/handle/11449/12879
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dc.contributor.authorFurtado, Kelly S.-
dc.contributor.authorPrado, Monize G.-
dc.contributor.authorAguiar e Silva, Marco A.-
dc.contributor.authorDias, Marcos C.-
dc.contributor.authorRivelli, Diogo P.-
dc.contributor.authorRodrigues, Maria Aparecida Marchesan-
dc.contributor.authorBarbisan, Luis Fernando-
dc.date.accessioned2014-05-20T13:37:16Z-
dc.date.accessioned2016-10-25T16:54:01Z-
dc.date.available2014-05-20T13:37:16Z-
dc.date.available2016-10-25T16:54:01Z-
dc.date.issued2012-11-01-
dc.identifierhttp://dx.doi.org/10.1111/j.1742-7843.2012.00903.x-
dc.identifier.citationBasic & Clinical Pharmacology & Toxicology. Hoboken: Wiley-blackwell, v. 111, n. 5, p. 339-347, 2012.-
dc.identifier.issn1742-7835-
dc.identifier.urihttp://hdl.handle.net/11449/12879-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/12879-
dc.description.abstractCoffee intake has been inversely related to the incidence of liver diseases, although there are controversies on whether these beneficial effects on human health are because of caffeine or other specific components in this popular beverage. Thus, this study evaluated the protective effects of coffee or caffeine intake on liver injury induced by repeated thioacetamide (TAA) administration in male Wistar rats. Rats were randomized into five groups: one untreated group (G1) and four groups (G2G5) treated with the hepatotoxicant TAA (200 similar to mg/kg b.w., i.p.) twice a week for 8 similar to weeks. Concomitantly, rats received tap water (G1 and G2), conventional coffee (G3), decaffeinated coffee (G4) or 0.1% caffeine (G5). After 8 similar to weeks of treatment, rats were killed and blood and liver samples were collected. Conventional and decaffeinated coffee and caffeine intake significantly reduced serum levels of alanine aminotransferase (ALT) (p similar to<similar to 0.001) and oxidized glutathione (p similar to<similar to 0.05), fibrosis/inflammation scores (p similar to<similar to 0.001), collagen volume fraction (p similar to<similar to 0.01) and transforming growth factor beta-1 (TGF-beta 1) protein expression (p similar to=similar to 0.001) in the liver from TAA-treated groups. In addition, conventional coffee and caffeine intake significantly reduced proliferating cellular nuclear antigen (PCNA) S-phase indexes (p similar to<similar to 0.001), but only conventional coffee reduced cleaved caspase-3 indexes (p similar to<similar to 0.001), active metalloproteinase 2 (p similar to=similar to 0.004) and the number of glutathione S-transferase placental form (GST-P)-positive preneoplastic lesions (p similar to<similar to 0.05) in the liver from TAA-treated groups. In conclusion, conventional coffee and 0.1% caffeine intake presented better beneficial effects than decaffeinated coffee against liver injury induced by TAA in male Wistar rats.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)-
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)-
dc.format.extent339-347-
dc.language.isoeng-
dc.publisherWiley-Blackwell-
dc.sourceWeb of Science-
dc.titleCoffee and Caffeine Protect against Liver Injury Induced by Thioacetamide in Male Wistar Ratsen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.description.affiliationUNESP São Paulo State Univ, Inst Biosci, Dept Morphol, BR-18618970 Botucatu, SP, Brazil-
dc.description.affiliationUNESP São Paulo State Univ, Sch Med, Dept Pathol, BR-18618970 Botucatu, SP, Brazil-
dc.description.affiliationUniv São Paulo, Sch Pharmaceut Sci, Dept Clin Chem & Toxicol, São Paulo, Brazil-
dc.description.affiliationUnespUNESP São Paulo State Univ, Inst Biosci, Dept Morphol, BR-18618970 Botucatu, SP, Brazil-
dc.description.affiliationUnespUNESP São Paulo State Univ, Sch Med, Dept Pathol, BR-18618970 Botucatu, SP, Brazil-
dc.description.sponsorshipIdFAPESP: 08/50985-5-
dc.description.sponsorshipIdFAPESP: 07/54858-5-
dc.description.sponsorshipIdFAPESP: 09/50890-7-
dc.description.sponsorshipIdCNPq: 474572/2008-0-
dc.description.sponsorshipIdCNPq: 301585/2009-1-
dc.identifier.doi10.1111/j.1742-7843.2012.00903.x-
dc.identifier.wosWOS:000309921600008-
dc.rights.accessRightsAcesso restrito-
dc.relation.ispartofBasic & Clinical Pharmacology & Toxicology-
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