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Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF‐κB activation and is a potent antiinflammatory compound in vivo

Sancho, Rocío ; Lucena, Concepción ; Macho, Antonio ; Calzado, Marco A. ; Blanco‐Molina, Magdalena ; Minassi, Alberto ; Appendino, Giovanni ; Muñoz, Eduardo

European journal of immunology, 2002-06, Vol.32 (6), p.1753-1763 [Periódico revisado por pares]

Weinheim: WILEY‐VCH Verlag GmbH

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  • Título:
    Immunosuppressive activity of capsaicinoids: capsiate derived from sweet peppers inhibits NF‐κB activation and is a potent antiinflammatory compound in vivo
  • Autor: Sancho, Rocío ; Lucena, Concepción ; Macho, Antonio ; Calzado, Marco A. ; Blanco‐Molina, Magdalena ; Minassi, Alberto ; Appendino, Giovanni ; Muñoz, Eduardo
  • Assuntos: Capsiate ; Inflammatory bowel disease ; NF‐κB ; Septic shock ; T cell
  • É parte de: European journal of immunology, 2002-06, Vol.32 (6), p.1753-1763
  • Notas: The first two authors contributed equally to this study.
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  • Descrição: Capsiate and its dihydroderivatives are the major capsaicinoids of sweet pepper. These new capsaicinoids do not activate the vanilloid receptor type 1 (VR1) but they share with capsaicin (CPS)some biological activities mediated in a VR1‐independent fashion. In this study we show that CPS and nordihydrocapsiate (CPT) inhibit early and late events in T cell activation, including CD69, CD25 and ICAM‐1 cell surface expression, progression to the S phase of the cell cycle and proliferation in response to TCR and CD28 co‐engagement. Moreover, both CPS and CPT inhibit NF‐κB activation in response to different agents including TNF‐α. CPS itself does not affect the DNA‐binding ability of NF‐κB but it prevents IκB kinase activation and IκBα degradation in a dose‐dependent manner, without inhibiting the activation of the mitogen‐activated protein kinases, p38, extracellular regulated kinase and c‐Jun N‐terminal protein kinase. Moreover, intraperitoneal pretreatment with CPT prevented mice from lethal septic shock induced by lipopolysaccharide. In a second model of inflammation CPT pretreatment greatly reduced the extensive damage in the glandular epithelium observed in the bowel of DSS‐treated mice. Taken together, these results suggest that CPT and related synthetic analogues target specific pathways involved in inflammation, and hold considerable potential for dietary health benefits as well as for pharmaceutical development.
  • Editor: Weinheim: WILEY‐VCH Verlag GmbH
  • Idioma: Inglês

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