Effects ofn-3 fatty acids on cartilage metabolism

Abstract

Although the clinical benefits of dietary supplementation withn-3 polyunsaturated fatty acids (PUFA) has been recognised for a number of years, the molecular mechanisms by which particular PUFA affect metabolism of cells within the synovial joint tissues are not understood. This study set out to investigate hown-3 PUFA and other classes of fatty acids affect both degradative and inflammatory aspects of metabolism of articular cartilage chondrocytes using anin vitromodel of cartilage degradation. Using well-established culture models, cartilage explants from normal bovine and human osteoarthritic cartilage were supplemented with eithern-3 orn-6 PUFA, and cultures were subsequently treated with interleukin 1 to initiate catabolic processes that mimic cartilage degradation in arthritis. Results show that supplementation specifically withn-3 PUFA, but notn-6 PUFA, causes a decrease in both degradative and inflammatory aspects of chondrocyte metabolism, whilst having no effect on the normal tissue homeostasis. Collectively, our data provide evidence supporting dietary supplementation ofn-3 PUFA, which in turn may have a beneficial effect of slowing and reducing inflammation in the pathogenesis of degenerative joint diseases in man.

Mechanical Stress and Nitric Oxide Influence Leukotriene Production in Cartilage

“…As shown in a previous investigation, however, articular cartilage can produce mRNA for 5-LOX and 12-LOX in response to fatty acids and interleukin 1 (22). In response to IL-1, however, LTB 4 is found at a barely detectable level (23).…”

Featured Article: Deficiency of G-protein coupled receptor 40, a lipid-activated receptor, heightens in vitro- and in vivo-induced murine osteoarthritis

“…From a nutritional point of view, omega-3 (n-3) PUFAs have been evidenced to modulate inflammation and cartilage degradation, 13,38,39 that contribute to prevent, slow down or rescue OA phenotype, and to improve mobility and activity. 11 With regards to our data pointing to a protective role of GPR40 in an OA context, and to the fact that fatty acids are well-known natural ligands of GPR40, one can speculate that these results originate from a GPR40 involvement.…”

Inspiré par les lipides (Médaille Chevreul 2014)

“…La destruction de cartilage par les protéases (mesurée par les glycosaminoglycanes) et la sécrétion d'une variété de cytokines (1L-1, TNF-α, etc.) ont été toutes les deux réduites à des niveaux indétectables en présence d'EPA et de DHA, partiellement en présence d'acide α-linolénique, mais aucunement avec un AGPI n-6 à longue chaîne l'acide arachidonique (Curtis et al, 2002 ;Zainal et al, 2009) (Fig. 6).…”