Cargando…
Dietary supplementation with arachidonic acid increases arachidonic acid content in paw, but does not affect arthritis severity or prostaglandin E(2) content in rat adjuvant-induced arthritis model
BACKGROUND: Arachidonic acid (ARA) is an essential fatty acid and a major constituent of biomembranes. It is converted into various lipid mediators, such as prostaglandin E(2) (PGE(2)), which is involved in the development of rheumatoid arthritis (RA). However, the effects of dietary ARA on RA are u...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4417218/ https://www.ncbi.nlm.nih.gov/pubmed/25595700 http://dx.doi.org/10.1186/1476-511X-14-3 |
Sumario: | BACKGROUND: Arachidonic acid (ARA) is an essential fatty acid and a major constituent of biomembranes. It is converted into various lipid mediators, such as prostaglandin E(2) (PGE(2)), which is involved in the development of rheumatoid arthritis (RA). However, the effects of dietary ARA on RA are unclear. Our objective was to clarify the effects of dietary ARA on an experimental rat arthritis model. METHODS: Lew rats were fed three contents of ARA diet (0.07%, 0.15% or 0.32% ARA in diet (w/w)), a docosahexaenoic acid (DHA) diet (0.32% DHA), or a control diet. After 4 weeks, arthritis was induced by injection of Freund’s complete adjuvant into the hind footpad. We observed the development of arthritis for another 4 weeks, and evaluated arthritis severity, fatty acid and lipid mediator contents in the paw, and expression of genes related to lipid mediator formation and inflammatory cytokines. Treatment with indomethacin was also evaluated. RESULTS: The ARA content of phospholipids in the paw was significantly elevated with dietary ARA in a dose-dependent manner. Dietary ARA as well as DHA did not affect arthritis severity (paw edema, arthritis score, and bone erosion). PGE(2) content in the paw was increased by arthritis induction, but was not modified by dietary ARA. Dietary ARA did not affect the contents of other lipid mediators and gene expression of cyclooxygenase (COX)-1, COX-2, lipoxgenases and inflammatory cytokines. Indomethacin suppressed arthritis severity and PGE(2) content in the paw. CONCLUSION: These results suggest that dietary ARA increases ARA content in the paw, but has no effect on arthritis severity and PGE(2) content of the paw in a rat arthritis model. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/1476-511X-14-3) contains supplementary material, which is available to authorized users. |
---|