CLA and EPA inhibit LPS-induced prostaglandin release from bovine endometrial cells through an NF-κB-dependent signaling mechanism

Although their action in antagonizing arachidonic acid metabolism is a key antiinflammatory effect of conjugated linoleic acid (CLA) and omega-3 polyunsaturated fatty acids (n-3 PUFA), these molecules have other antiinflammatory effects that might occur upstream of altered eicosanoid production. We examined the effects of two CLA isomers (c9, t11 and t10, c12 isomers), n-3 PUFA (EPA and DHA), and kappa NF-kappa B inhibitor (ammonium pyrrolidine dithiocarbamate (PDTC)) on lipopolysaccharide (LPS)-induced secretion of prostaglandins (PGE(2) and PGF(2a)) by bovine endometrial (BEND) cells. LPS increased PGE(2) and PGF(2a) concentrations in BEND cell-conditioned media in a concentration-and time-dependent manner. The c9, t11 CLA isomer and EPA decreased prostaglandin response to LPS. Addition of PDTC, alone or in combination with c9, t11 CLA or EPA, inhibited LPS-induced eicosanoid release into the culture medium. Results indicate that the c9, t11 CLA isomer and EPA inhibit the endometrial prostaglandin release in cattle and that these molecules may act through an NF-kappa B signaling mechanism.