Ikarisoside A inhibits inducible nitric oxide synthase in lipopolysaccharide-stimulated RAW 264.7 cells via p38 kinase and nuclear factor-κB signaling pathways

This study examined the anti-inflammatory properties of Ikarisoside A, isolated from Epimedium koreanum (Berberidaceae), in lipopolysaccharide (LPS)-stimulated macrophages. Ikarisoside A inhibited the expression of LPS-stimulated inducible nitric oxide synthase (iNOS) and the production of nitric oxide (NO) in LPS-stimulated RAW 264.7 cells and mouse bone marrow-derived macrophages (BMMs) in a concentration-dependent manner. In addition, Ikarisoside A reduced the release of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). Furthermore, Ikarisoside A inhibited the activity of p38 kinase and nuclear factor-κB (NF-κB), which are signaling molecules involved in NO production. NO production was inhibited when the cells were treated with LPS and either SB 203580 (a p38 inhibitor) or Bay 11-7082 (an inhibitory κB kinase 2 inhibitor). These results suggest that Ikarisoside A inhibits the production of NO by inhibiting the activity of p38 MAPK and NF-κB. As a result of these properties, Ikarisoside A has the potential to be used as an effective anti-inflammatory agent.