Produção Nacional
Revisado por pares
Blockade of leukotriene B4 prevents articular incapacitation in rat zymosan-induced arthritis
2004; Elsevier BV; Volume: 497; Issue: 1 Linguagem: Inglês
10.1016/j.ejphar.2004.06.025
ISSN1879-0712
AutoresFrancisco Airton Castro Rocha, Mauro Martins Teixeira, José Rocha, Virgínia Cláudia Carneiro Girão‐Carmona, Mirna Marques Bezerra, Ronaldo de Albuquerque Ribeiro, Fernando Q. Cunha,
Tópico(s)Asthma and respiratory diseases
ResumoWe investigated whether leukotrienes mediate cell influx and articular incapacitation in zymosan-induced arthritis. Rats received 1 mg zymosan intra-articularly (i.a.). The hyperalgesia was measured using the rat articular incapacitation test. Cell influx, leukotriene B4 and prostaglandin E2 levels were assessed in the joint exudate, at 6 h. Groups received either the leukotriene B4 synthesis inhibitor MK 886 (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl)]-2,2-dimethylpropanoic acid 30 min before or 2 h after the zymosan; 0.3–3 mg kg−1 i.p.), the leukotrienes synthesis inhibitor BWA4C (N-(3-phenoxycinnamyl)-acetohydroxamic acid—2 h after the zymosan; 10 μg i.a.) or the peptido-leukotrienes antagonist sodium montelukast (30 min before and 2 h after the zymosan; 10 mg kg−1 per os). MK 886 inhibited the articular incapacitation and cell influx, while reducing leukotriene B4, but not prostaglandin E2 levels. BWA4C inhibited the articular incapacitation. Sodium montelukast did not affect either of the parameters. The data suggest that leukotriene B4 is involved in cell influx and articular incapacitation in zymosan arthritis.
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