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Doctoral Thesis
DOI
10.11606/T.42.2007.tde-24092007-094137
Document
Author
Full name
Aila Mirtes Teles
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2007
Supervisor
Committee
Costa, Soraia Kátia Pereira (President)
Antunes, Edson
Lima, Wothan Tavares de
Martins, Rodrigo Alvaro Brandão Lopes
Paschoal, Sisi Marcondes
Title in Portuguese
Contribuição farmacológica à gênese da inflamação neurogênica em vias aéreas de ratos frente a dois poluentes: Partículas eliminadas na exaustão do diesel (PED) e 1,2-naftoquinona (1,2-NQ).
Keywords in Portuguese
1 2-naftoquinona
Capsaicina
Inflamação neurogênica
Partículas de exaustão do diesel
Receptor TRPV1
Vias aéreas de rato
Abstract in Portuguese
Neste estudo efetuou-se uma análise comparativa da resposta inflamatória e estresse oxidativo produzido pela administração intratraqueal (i.tr.) das PED e/ou 1,2-NQ em vias aéreas de ratos. O efeito destes poluentes sobre a funcionabilidade dos macrófagos foi também avaliado. A injeção i.tr. das PED, numa dose incapaz de causar edema, promoveu efeito aditivo no edema e influxo de leucócitos induzido pela 1,2-NQ nas vias aéreas. O edema foi inibido por antagonistas de taquicininas ou capsaicina, mas o influxo de leucócitos não. O tratamento com estes poluentes aumentou a expressão gênica dos receptores TRPV1, taquicininas e TNFR1, as quais foram reduzidas, mas a iNOS aumentada, em animais depletados de neuropeptídeos. Concentrações elevadas de citocinas pró-inflamatórias foram encontradas no brônquio de ratos saudáveis e, mais intensamente, naqueles tratados com capsaicina. Níveis basais de 3-NT, IL-10 ou IFN-?? no brônquio não foram alterados pelos poluentes. A fagocitose de partículas de zimosan foi aumentada após a exposição de animais saudáveis e depletados de neuropeptídeos aos poluentes. A inflamação nas vias aéreas de ratos expostos ao MP do diesel é influenciada por concentrações de 1,2-NQ no ambiente, via mecanismo neurogênico.
Title in English
Pharmacological contribution to the genese of neurogenic inflammation in the rat airways evoked by two ambient pollutants: diesel exhaust particles (DEP) and 1,2-naphthoquinone (1,2-NQ).
Keywords in English
1 2-naphthoquinone
Capsaicin
Neurogenic inflammation
Niesel exhaust particles
Rat airways
TRPV1 receptor
Abstract in English
Pharmacological approaches on the healthy side effects evoked by the interaction between environmental pollutants are poorly studied. Here we tested the hypothesis that the environmental chemical 1,2-naphthoquinone (1,2-NQ) is implicated in the exacerbation of airways diseases induced by exposure to diesel exhaust particles (DEP), and that involves a neurogenic-mediated mechanism. Intra-tracheal (i.tr.) injection of DEP (1 and 5 mg/kg) or 1,2-NQ (35 and 100 nmol/kg) caused oedema in rat airways. DEP (at a dose unable to produce oedema) increased the 1,2-NQ-induced responses in the rat airways in a additive manner. This effect was reduced by L-732,138, an NK1 receptor antagonist, and in a lesser extent by the NK2 receptor SR48968. Capsaicin treatment also markedly reduced pollutants-induced oedema. Exposure to pollutants increased the TRPV1, NK1 and NK2 receptors gene expression in bronchus, an effect nearly abolished by capsaicin treatment. No evidence of increased 3-NT in main bronchus was found. Our results are consistent with the hypothesis that DEP-induced airways oedema is highly influenced by increased ambient levels of 1,2-NQ, and takes place by neurogenic-mediated mechanisms involving up-regulation of TRPV1 and tachykinin receptors.
 
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Publishing Date
2007-10-22
 
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