Both adiponectin and interleukin-10 inhibit LPS-induced activation of the NF-kappa B pathway in 3T3-L1 adipocytes

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dc.contributor.authorLira, Fábio Santos de [UNIFESP]
dc.contributor.authorRosa Neto, José Cesar [UNIFESP]
dc.contributor.authorPimentel, Gustavo Duarte [UNIFESP]
dc.contributor.authorSeelaender, Marilia
dc.contributor.authorDâmaso, Ana Raimunda [UNIFESP]
dc.contributor.authorOyama, Lila Missae [UNIFESP]
dc.contributor.authorNascimento, Claudia Maria da Penha Oller do [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.date.accessioned2016-01-24T14:17:35Z
dc.date.available2016-01-24T14:17:35Z
dc.date.issued2012-01-01
dc.description.abstractAdiponectin and interleukin 10 (IL-10) are adipokines that are predominantly secreted by differentiated adipocytes and are involved in energy homeostasis, insulin sensitivity, and the anti-inflammatory response. These two adipokines are reduced in obese subjects, which favors increased activation of nuclear factor kappa B (NF-kappa B) and leads to elevation of pro-inflammatory adipokines. However, the effects of adiponectin and IL-10 on NF-kappa B DNA binding activity (NF-kappa Bp50 and NF-kappa Bp65) and proteins involved with the toll-like receptor (TLR-2 and TLR-4) pathway, such as MYD88 and TRAF6 expression, in lipopolysaccharide-treated 3T3-L1 adipocytes are unknown. Stimulation of lipopolysaccharide-treated 3T3-L1 adipocytes for 24 h elevated IL-6 levels; activated the NF-kappa B pathway cascade; increased protein expression of IL-6R, TLR-4, MYD88, and TRAF6; and increased the nuclear activity of NF-kappa B (p50 and p65) DNA binding. Adiponectin and IL-10 inhibited the elevation of IL-6 levels and activated NF-kappa B (p50 and p65) DNA binding. Taken together, the present results provide evidence that adiponectin and IL-10 have an important role in the anti-inflammatory response in adipocytes. in addition, inhibition of NF-kappa B signaling pathways may be an excellent strategy for the treatment of inflammation in obese individuals. (C) 2011 Elsevier B.V. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Fis, BR-04023060 São Paulo, Brazil
dc.description.affiliationUniv São Paulo, Inst Biomed Sci, Canc & Metab Grp, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Fis, BR-04023060 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIDFAPESP: 08/54733-0
dc.format.extent98-106
dc.identifierhttps://dx.doi.org/10.1016/j.cyto.2011.10.001
dc.identifier.citationCytokine. London: Academic Press Ltd- Elsevier B.V., v. 57, n. 1, p. 98-106, 2012.
dc.identifier.doi10.1016/j.cyto.2011.10.001
dc.identifier.fileWOS000299580800016.pdf
dc.identifier.issn1043-4666
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/34340
dc.identifier.wosWOS:000299580800016
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofCytokine
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectAdiponectinen
dc.subjectInterleukin 10en
dc.subject3T3-L1en
dc.subjectLipopolysaccharideen
dc.subjectNF-kappa B pathwayen
dc.titleBoth adiponectin and interleukin-10 inhibit LPS-induced activation of the NF-kappa B pathway in 3T3-L1 adipocytesen
dc.typeinfo:eu-repo/semantics/article
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