PAF modulates eicosanoids and TNF release in immune-complex arthritis in rats

PAF modulates eicosanoids and TNF release in immune-complex arthritis in rats

Autor Rocha, FAC Google Scholar
Andrade, LEC Google Scholar
Russo, M. Google Scholar
Jancar, S. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Resumo The participation of lipid mediators and tumor necrosis factor (TNF) on an experimental model of immune-complex arthritis was investigated. Male Wistar rats received intraarticular injection of rabbit antibodies to bovine serum albumin into the knee joint followed by i.v. injection of the antigen. the levels of eicosanoids and TNF released into the synovial exudates were then assessed using ELISA and the L929 lytic cell assay, respectively. Increase in the levels of LTB4, TXB2 and PGE2 were detected 5 min, 5 min, and 6 h after arthritis induction, respectively. Pretreatment with the PAF receptor antagonist WEB 2170 decreased the levels of PGE2 and increased those of LTB4, without altering TXB2 levels. Increase in the levels of TNF was detected at 3 h of arthritis. Pretreatment with either the cycloxygenase inhibitor indomethacin or the 5-lipoxygenase inhibitor L-663,536 had no effect on TNF levels. Pretreatment with WEB 2170 significantly decreased TNF levels. These results are the first demonstration of eicosanoids and TNF release in immune-complex arthritis. the data also suggest that PAF had both a positive and negative modulatory role on the release of PGE2 and LTB4, respectively. Moreover,TNF release into the synovial exudate did not depend on eicosanoids whereas platelet activating factor (PAF) appeared to mediate the release of this cytokine in the model. (C) 1997 Elsevier Science B.V.
Palavra-chave arthritis
arthus reactions
eicosanoids
platelet activating factor
tumor necrosis factor
Idioma Inglês
Data de publicação 1997-05-01
Publicado em Journal of Lipid Mediators and Cell Signalling. Amsterdam: Elsevier B.V., v. 16, n. 1, p. 1-10, 1997.
ISSN 0929-7855 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 1-10
Fonte http://dx.doi.org/10.1016/S0929-7855(96)00563-9
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:A1997WQ58900001
Endereço permanente http://repositorio.unifesp.br/handle/11600/25721

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