dc.contributorUniversidade Estadual Paulista (Unesp)
dc.creatorNogueira, M. N. M. [UNESP]
dc.creatorAquino, S. G. [UNESP]
dc.creatorRossa Júnior, Carlos [UNESP]
dc.creatorSpolidório, Denise Madalena Palomari [UNESP]
dc.date2015-03-18T15:52:55Z
dc.date2015-03-18T15:52:55Z
dc.date2014-09-01
dc.date.accessioned2023-09-09T11:01:34Z
dc.date.available2023-09-09T11:01:34Z
dc.identifierhttp://dx.doi.org/10.1007/s00011-014-0749-x
dc.identifierInflammation Research. Basel: Springer Basel Ag, v. 63, n. 9, p. 769-778, 2014.
dc.identifier1023-3830
dc.identifierhttp://hdl.handle.net/11449/116242
dc.identifier10.1007/s00011-014-0749-x
dc.identifierWOS:000340557100007
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8765729
dc.descriptionTea tree oil (TTO) is an essential oil with anti-inflammatory properties, steam distilled from the plant Melaleuca alternifolia. We investigated the immunomodulatory properties of TTO and its components (terpinen-4-ol and alpha-terpineol) using lipopolysaccharide (LPS)-stimulated macrophages.The ability of TTO, terpinen-4-ol and alpha-terpineol to modulate the macrophage response to bacterial LPS stimulation was assessed by ELISA for tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6 and IL-10 cytokine production and by western blotting for the activation of nuclear factor kappa B (NF-kappa B) and p38 mitogen-activated protein kinase (MAPK) signaling, which are associated with the expression of pro-inflammatory cytokines. We used a human monocytic cell line (U937) differentiated into macrophages.LPS induced the production of all cytokines, and TTO and its components significantly reduced the production of IL-1 beta, IL-6 and IL-10. The production of TNF-alpha was not affected by either TTO or its major components. The modulation of cytokine production was not mediated by changes in NF-kappa B or p38 MAPK activation.TTO, terpinen-4-ol and alpha-terpineol can suppress the production of inflammatory mediators in LPS-stimulated human macrophages; this inhibition was mediated by interfering with the NF-kB, p38 or ERK MAPK pathways.
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionUNESP, Dept Diag & Surg, Sch Dent Araraquara, Araraquara, SP, Brazil
dc.descriptionUNESP, Dept Physiol & Pathol, Sch Dent Araraquara, Araraquara, SP, Brazil
dc.descriptionUNESP, Dept Diag & Surg, Sch Dent Araraquara, Araraquara, SP, Brazil
dc.descriptionUNESP, Dept Physiol & Pathol, Sch Dent Araraquara, Araraquara, SP, Brazil
dc.descriptionFAPESP: 09/54190-0
dc.descriptionFAPESP: 10/18968-3
dc.format769-778
dc.languageeng
dc.publisherSpringer
dc.relationInflammation Research
dc.relation2.990
dc.relation1,062
dc.rightsAcesso restrito
dc.sourceWeb of Science
dc.subjectTea tree oil
dc.subjectMacrophages
dc.subjectCytokines
dc.subjectInflammation
dc.titleTerpinen-4-ol and alpha-terpineol (tea tree oil components) inhibit the production of IL-1 beta, IL-6 and IL-10 on human macrophages
dc.typeArtigo


Este ítem pertenece a la siguiente institución