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Registro Completo |
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Biblioteca(s): |
Embrapa Suínos e Aves. |
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Data corrente: |
24/04/2015 |
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Data da última atualização: |
24/04/2015 |
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Tipo da produção científica: |
Artigo em Anais de Congresso |
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Autoria: |
MARCHESI, J. A. P.; IBELLI, A. M. G.; PALUDO, E.; TAVERNARI, F. de C.; PEIXOTO, J. de O.; LEDUR, M. C. |
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Afiliação: |
JORGE AUGUSTO PETROLI MARCHESI, UNC; ADRIANA MERCIA GUARATINI IBELLI, CNPSA; EDIANE PALUDO, UDESC; FERNANDO DE CASTRO TAVERNARI, CNPSA; JANE DE OLIVEIRA PEIXOTO, CNPSA; MONICA CORREA LEDUR, CNPSA. |
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Título: |
Expressão do gene receptor da leptina (LEPR) em frangos de corte normais e afetados pela necrose da cabeça do fêmur. |
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Ano de publicação: |
2014 |
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Fonte/Imprenta: |
In: JORNADA DE INICIAÇÃO CIENTÍFICA, 8., 2014, Concórdia. Anais... Brasília: Embrapa, 2014. p. 43-44 JINC 2014. |
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Idioma: |
Português |
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Palavras-Chave: |
Gene receptor da leptina (LEPR); Necrose da cabeça do fêmur. |
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Thesagro: |
Avicultura; Genética. |
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Categoria do assunto: |
-- |
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URL: |
https://ainfo.cnptia.embrapa.br/digital/bitstream/item/122728/1/final7646.pdf
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Marc: |
LEADER 00760nam a2200205 a 4500
001 2014134
005 2015-04-24
008 2014 bl uuuu u00u1 u #d
100 1 $aMARCHESI, J. A. P.
245 $aExpressão do gene receptor da leptina (LEPR) em frangos de corte normais e afetados pela necrose da cabeça do fêmur.$h[electronic resource]
260 $aIn: JORNADA DE INICIAÇÃO CIENTÍFICA, 8., 2014, Concórdia. Anais... Brasília: Embrapa, 2014. p. 43-44 JINC 2014.$c2014
650 $aAvicultura
650 $aGenética
653 $aGene receptor da leptina (LEPR)
653 $aNecrose da cabeça do fêmur
700 1 $aIBELLI, A. M. G.
700 1 $aPALUDO, E.
700 1 $aTAVERNARI, F. de C.
700 1 $aPEIXOTO, J. de O.
700 1 $aLEDUR, M. C.
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Registro original: |
Embrapa Suínos e Aves (CNPSA) |
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 | Acesso ao texto completo restrito à biblioteca da Embrapa Gado de Leite. Para informações adicionais entre em contato com cnpgl.biblioteca@embrapa.br. |
Registro Completo
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Biblioteca(s): |
Embrapa Gado de Leite. |
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Data corrente: |
14/03/2013 |
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Data da última atualização: |
09/02/2024 |
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Tipo da produção científica: |
Artigo em Periódico Indexado |
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Circulação/Nível: |
A - 2 |
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Autoria: |
MAZZOCCOLI, L.; CARDOSO, SILVIA H.; AMARANTE, G. W.; SOUZA, M. V. N. DE; DOMINGUES, R.; MACHADO, M. A.; ALMEIDA, M. V. DE; TEIXEIRA, H. C. |
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Afiliação: |
LUCIANO MAZZOCCOLI, UFJF; SILVIA H. CARDOSO, UFJF; GIOVANNI W. AMARANTE, UFJF; MARCUS V. N. DE SOUZA, UFJF; ROBERT DOMINGUES, CPPSUL; MARCO ANTONIO MACHADO, CNPGL; MAURO V. DE ALMEIDA, UFJF; HENRIQUE C. TEIXEIRA, UFJF. |
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Título: |
Novel thalidomide analogues from diamines inhibit pro-inflammatory cytokine production and CD80 expression while enhancing IL-10. |
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Ano de publicação: |
2012 |
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Fonte/Imprenta: |
Biomedicine & Pharmacotherapy, v. 66, p. 323-329, 2012. |
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DOI: |
https://doi.org/10.1016/j.biopha.2012.05.001 |
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Idioma: |
Inglês |
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Notas: |
Não consta da meta de 2012. |
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Conteúdo: |
Thalidomide is used to treat a variety of diseases including erythema nodosum leprosum, an inflammatory complication of leprosy. However, this drug has severe teratogenic activity and novel thalidomide analogues might be used to treat diseases without this severe side effect. A series of diamine compounds containing two hydrolyzed phthalimide units were chosen as analogues of thalidomide and evaluated regarding their capacity to regulate the production of molecules involved in inflammatory responses. TNF-α, IL-12 and IL-10 production, and the expression of CD80 and CD86 were investigated in LPS plus IFN-γ-stimulated J774A.1 cells by ELISA and flow cytometry, respectively. The expression of TNF-α and IL-10 mRNA was analyzed by real time RT-PCR. TNF-α, IL-6, IFN-γ, CXCL9 and CXCL10 production by human peripheral blood mononuclear cells (PBMC) were evaluated by flow cytometry. Compounds 3, 6 and 9 greatly inhibited TNF-α and IL-12 production while enhancing IL-10. In addition, CD80 expression was inhibited, but not CD86. The compounds inhibited TNF-α production by PBMC more than thalidomide and also had an inhibitory effect on the production of IL-6, IFN-γ, CXCL9 and CXCL10. Levels of mRNA for TNF-α were reduced after treatment with the compounds, suggesting post- transcriptional effects. The compounds had no effect on cell viability. Our results indicate that the novel diamine compounds 3, 6 and 9 inhibit critical pro-inflammatory cytokines and stimulate IL-10, which make them attractive candidate drugs for the treatment of certain inflammatory conditions and cancer. MenosThalidomide is used to treat a variety of diseases including erythema nodosum leprosum, an inflammatory complication of leprosy. However, this drug has severe teratogenic activity and novel thalidomide analogues might be used to treat diseases without this severe side effect. A series of diamine compounds containing two hydrolyzed phthalimide units were chosen as analogues of thalidomide and evaluated regarding their capacity to regulate the production of molecules involved in inflammatory responses. TNF-α, IL-12 and IL-10 production, and the expression of CD80 and CD86 were investigated in LPS plus IFN-γ-stimulated J774A.1 cells by ELISA and flow cytometry, respectively. The expression of TNF-α and IL-10 mRNA was analyzed by real time RT-PCR. TNF-α, IL-6, IFN-γ, CXCL9 and CXCL10 production by human peripheral blood mononuclear cells (PBMC) were evaluated by flow cytometry. Compounds 3, 6 and 9 greatly inhibited TNF-α and IL-12 production while enhancing IL-10. In addition, CD80 expression was inhibited, but not CD86. The compounds inhibited TNF-α production by PBMC more than thalidomide and also had an inhibitory effect on the production of IL-6, IFN-γ, CXCL9 and CXCL10. Levels of mRNA for TNF-α were reduced after treatment with the compounds, suggesting post- transcriptional effects. The compounds had no effect on cell viability. Our results indicate that the novel diamine compounds 3, 6 and 9 inhibit critical pro-inflammatory cytokines and stimulate IL-10, which make them... Mostrar Tudo |
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Palavras-Chave: |
IL-10; Resposta inflamatória; Talidomida analógico; TNF-a. |
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Categoria do assunto: |
H Saúde e Patologia |
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Marc: |
LEADER 02493naa a2200277 a 4500
001 1953088
005 2024-02-09
008 2012 bl uuuu u00u1 u #d
024 7 $ahttps://doi.org/10.1016/j.biopha.2012.05.001$2DOI
100 1 $aMAZZOCCOLI, L.
245 $aNovel thalidomide analogues from diamines inhibit pro-inflammatory cytokine production and CD80 expression while enhancing IL-10.$h[electronic resource]
260 $c2012
500 $aNão consta da meta de 2012.
520 $aThalidomide is used to treat a variety of diseases including erythema nodosum leprosum, an inflammatory complication of leprosy. However, this drug has severe teratogenic activity and novel thalidomide analogues might be used to treat diseases without this severe side effect. A series of diamine compounds containing two hydrolyzed phthalimide units were chosen as analogues of thalidomide and evaluated regarding their capacity to regulate the production of molecules involved in inflammatory responses. TNF-α, IL-12 and IL-10 production, and the expression of CD80 and CD86 were investigated in LPS plus IFN-γ-stimulated J774A.1 cells by ELISA and flow cytometry, respectively. The expression of TNF-α and IL-10 mRNA was analyzed by real time RT-PCR. TNF-α, IL-6, IFN-γ, CXCL9 and CXCL10 production by human peripheral blood mononuclear cells (PBMC) were evaluated by flow cytometry. Compounds 3, 6 and 9 greatly inhibited TNF-α and IL-12 production while enhancing IL-10. In addition, CD80 expression was inhibited, but not CD86. The compounds inhibited TNF-α production by PBMC more than thalidomide and also had an inhibitory effect on the production of IL-6, IFN-γ, CXCL9 and CXCL10. Levels of mRNA for TNF-α were reduced after treatment with the compounds, suggesting post- transcriptional effects. The compounds had no effect on cell viability. Our results indicate that the novel diamine compounds 3, 6 and 9 inhibit critical pro-inflammatory cytokines and stimulate IL-10, which make them attractive candidate drugs for the treatment of certain inflammatory conditions and cancer.
653 $aIL-10
653 $aResposta inflamatória
653 $aTalidomida analógico
653 $aTNF-a
700 1 $aCARDOSO, SILVIA H.
700 1 $aAMARANTE, G. W.
700 1 $aSOUZA, M. V. N. DE
700 1 $aDOMINGUES, R.
700 1 $aMACHADO, M. A.
700 1 $aALMEIDA, M. V. DE
700 1 $aTEIXEIRA, H. C.
773 $tBiomedicine & Pharmacotherapy$gv. 66, p. 323-329, 2012.
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