Avaliação da Atividade do Ácido Pimaradienóico na Sinalização de Mastócitos

• Autor(a) principal: Souza, Anderson Roberto de
• Data de Publicação: 2013
• Tipo de documento: Dissertação
• Idioma: por
• Título da fonte: Repositório do Centro Universitário Braz Cubas
• Texto Completo: https://repositorio.cruzeirodosul.edu.br/handle/123456789/788
• topic: Ácido Pimaradienôico; Mastócitos; Inflamação; Desgranulação; Sinalização dos mastócitos; CNPQ::CIENCIAS EXATAS E DA TERRA::QUIMICA::QUIMICA ORGANICA

Activation of mast cells via high affinity receptor FcεRI initiates a cascade of signaling events, in its turn, leads to secretion of mediators from granules of mast cells. These mediators play a key role in the inflammatory process and consequently in response to allergens. Thus, the non-activation of mast cells is an intended effect when an anti-inflammatory drug is used in a specific therapy. Thereby, studying mast cells represent an important way for development of new drugs for the treatment of several pathologies. Therefore, this study aimed to analyze the behavior of mast cells when incubated in the presence of diterpene acid pimaradienóico (AP). Signaling events mediated by IgE on mast cells lead to the increase of intracellular Ca2+ concentration, which causes the activation of these cells. This study aimed to evaluate the role of (AP) on the activation of mast cells which release preformed factors and are present in the secretory granules of mast cells. We also evaluated the effect of AP on transcription via of both NFAT and NFkB in RBL-2H3NFAT-GFP and RBL-2H3NFkB-GFP cells. NFAT and NFkB acts on the synthesis of the mast cells neo-synthesized factors. Results demonstrated that AP did not activate mast cells via receptor FcεRI from the incubation with cell lineage NFkB2 and V9 and does not occurs activation of the transcription factors NFAT and NF-kB. We conclude that the AP can be regarded as a possible prototype for a future drug used to aid in the treatment of pathologies which involving the activation of inflammatory pathways.