Omega-3 fatty acids, which are found in marine organisms, have been associated with beneficial health effects. One mechanism for their anti-inflammatory effect is via competitive inhibition of the enzymatic activity of cyclooxygenase (COX), which is the rate-limiting step in the biosynthesis of prostaglandins. Massaro et al. report that exposure of vascular endothelial cells to the omega-3 fatty acid docosahexaenoate (DHA) for periods long enough for it to be incorporated into cellular membranes inhibits the activation of nuclear factor 
B (NF-B) and, subsequently, the expression of COX-2 and prostaglandin production in response to the proinflammatory signal interleukin-1
(IL-1). Treatment of endothelial cells with DHA altered their responses to IL-1 by (i) decreasing the activation of extracellular-stimulated kinases 1 and 2, without changing the activation of p38 mitogen-activated protein kinase; (ii) decreasing reactive oxygen species production through inhibiting the membrane association of the p47phox subunit of NADPH oxidase, and (iii) decreasing the membrane association of protein kinase C
(PKC), but not PKC or PKC
. Thus, it appears that the benefits of omega-3 fatty acids may be due in part to their effects on membrane lipid composition, which reduces signaling in response to inflammatory stimuli. -- NRG
Proc. Natl. Acad. Sci. U.S.A. 103, 15184 (2006).
