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Leukotriene B(4) limits the effectiveness of fish oil in an animal model of asthma

This study aimed to evaluate the levels of eicosanoids derived from arachidonic acid (ARA) in the lungs of asthmatic rats supplemented with fish oil. The present data gives insight into the action of fish oil in asthma, related to its inability to modify the contractile capacity of tracheal smooth m...

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Detalles Bibliográficos
Autores principales: Miranda, D.T.S.Z., Zanatta, A.L., Miles, E.A., Calder, P.C., Nishiyama, A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8591350/
https://www.ncbi.nlm.nih.gov/pubmed/34816034
http://dx.doi.org/10.1016/j.heliyon.2021.e08326
Descripción
Sumario:This study aimed to evaluate the levels of eicosanoids derived from arachidonic acid (ARA) in the lungs of asthmatic rats supplemented with fish oil. The present data gives insight into the action of fish oil in asthma, related to its inability to modify the contractile capacity of tracheal smooth muscle reported previously in a model of asthma in rats. Male Wistar rats were supplemented daily with 1 g of fish oil/kg of body weight for 21 days. They were exposed to ovalbumin (OVA) after previous sensitization with OVA to induce asthma. Pulmonary levels of five eicosanoids were measured using immunoassay kits: PGE(2), TXB(2), LTB(4), LXA(4), and 8-iso PGF(2α). In asthmatic rats, supplementation with fish oil resulted in lower concentrations of lung eicosanoids produced by cyclooxygenase-2 and 15-lipoxygenase: PGE(2), TXB(2), and LXA(4), respectively. Fish oil supplementation also decreased the non-enzymatically produced eicosanoid 8-iso PGF(2α). Fish oil supplementation did not affect LTB(4), a metabolite of 5-lipoxygenase. The limited efficacy of fish oil supplementation in asthmatic rats is associated with a lack of action in reducing the levels of LTB(4) in the lungs. Thus, fish oil differentially modulates the concentrations of eicosanoids derived from ARA via specific pathways in an animal model of asthma.