Decreased production of inflammatory mediators in human osteoarthritic chondrocytes by conjugated linoleic acids

Osteoarthritic chondrocytes (OC) produce excessive prostaglandin E-2 (PGE(2)) and nitric oxide (NO), which function as inflammation mediators in the pathogenesis of osteoarthritis (OA). This study examined the effect of CLA alone and in combination with other PUFA on the FA composition and the production of PGE(2) and NO in OC cultures isolated from OA patients. Human OC were grown in monolayer and treated with one of the following PUFA treatments: CLA, CLA + arachidonic acid (CLA/AA), CLA + EPA (CLA/EPA), linoleic acid (LA), LA + AA (LA/AA), LA + EPA (LA/EPA), and ethanol (as a vehicle control) at 10 and 20 PM for 6 d. Supplementation of PUFA at 10 muM for 6 d did not introduce any cytotoxic effects or morphological changes in OC, whereas 20 muM resulted in apoptosis. Cultures of OC treated with CLA, CLA/AA, and CLA/EPA had higher concentrations of CLA isomers, and these isomers were not detected in other treatments. Supplementation of CLA or LA alone to the OC led to a lower PGE(2) production compared to the control. Combination of CLA/EPA resulted in the lowest PGE(2) production in cultured OC. OC cultures treated with CLA were lower in NO production than the control, whereas the LA/AA treatment demonstrated the lowest NO production. The fact that CLA alone or in combination with other PUFA modulated PGE(2) and NO production in human OC cultures suggests that these 18:2 isomers may have the potential to influence OA pathogenesis.