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  • Title: Ikarisoside A inhibits inducible nitric oxide synthase in lipopolysaccharide-stimulated RAW 264.7 cells via p38 kinase and nuclear factor-kappaB signaling pathways.
    Author: Choi HJ, Eun JS, Park YR, Kim DK, Li R, Moon WS, Park JM, Kim HS, Cho NP, Cho SD, Soh Y.
    Journal: Eur J Pharmacol; 2008 Dec 28; 601(1-3):171-8. PubMed ID: 18929556.
    Abstract:
    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-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Furthermore, Ikarisoside A inhibited the activity of p38 kinase and nuclear factor-kappaB (NF-kappaB), 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 kappaB kinase 2 inhibitor). These results suggest that Ikarisoside A inhibits the production of NO by inhibiting the activity of p38 MAPK and NF-kappaB. As a result of these properties, Ikarisoside A has the potential to be used as an effective anti-inflammatory agent.
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