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-${kappa}B$ (NF-${kappa}B$) into the nucleus in immunocytochemical analysis for NF-${kappa}B$ 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-${alpha}$), and prostaglandin $E_2$ ($PGE_2$) 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-${alpha}$, and $PGE_2$ in activated Raw 264.7 cells through NF-${kappa}B$-dependent pathways.