(-)-pinoresinol monomethyl ether inhibits LPS-induced iNOS and Cox-2 expression via the attenuation of NF-κb in Raw 264.7 macrophage cells

Abstract

Anti-inflammatory effects of (-)-pinoresinol monomethyl ether (PME) were evaluated on lipopolysaccharide (LPS)-treated Raw 264.7 macrophage cells. PME inhibited translocation of p65-nuclear factor-κB (NF-κB) into the nucleus in immunocytochemical analysis for NF-κB activation, expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in Western blotting, as well as production of pro-inflammatory mediators, such as nitric oxide (NO), tumor necrosis factor (TNF-α), and prostaglandin E2 (PGE2) in LPS-induced Raw 264.7 cells. These results suggest the anti-inflammatory activity of PME could be due to the down-regulation of iNOS, COX-2, TNF-α, and PGE2 in activated Raw 264.7 cells through NF-κB-dependent pathways.