The essential oil isolated from Artemisia capillaris prevents LPS-induced production of NO and PGE(2) by inhibiting MAPK-mediated pathways in RAW 264.7 macrophages.
Artemisia capillaris (A. capillaris) is used in traditional Korean herbal medicine for its believedanti-inflammatory activities. Previous studies have suggested that the essential oil of A. capillaris contains the active components responsible for its pharmacological effect, even though the mechanism for its action is unclear. This study examined the inhibitory effects of the essential oil of A. capillaris on the lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and prostaglandin E(2) (PGE(2)). The essential oil significantly inhibited the production of NO in the LPS-stimulated RAW 264.7 macrophages, which was mediated by the down-regulation of inducible NO synthase (iNOS) expression but not by its direct cytotoxic activity. The essential oil also blocked the secretion of PGE(2) and the expression of cyclooxygenase-2 (COX-2) in the LPS-stimulated cells. Western blot analysis showed that the essential oil inhibited the phosphorylation of IkappaB-alpha, nuclear translocation of p65, and subsequent activation of NF-kappaB. In addition, the essential oil suppressed the LPS-stimulated activation of mitogen-activated protein kinases (MAPKs) as well as the AP-1 DNA-binding activity. Moreover, MAPK inhibitors significantly reduced the LPS-induced production of NO and PGE(2). Collectively, we suggest that the oil inhibits the expression and production of inflammatory mediators by blocking the MAPK-mediated pathways and inhibiting the activation of NF-kappaB and AP-1.
Cha
Jeong-Dan
JD
Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul, Korea.
Moon
Sang-Eun
SE
Kim
Hye-Young
HY
Lee
Jeong-Chae
JC
Lee
Kyung-Yeol
KY
D000818:Animals; D019306:Artemisia / Q000737:chemistry* / Q000145:classification; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000187:drug effects; D015232:Dinoprostone / Q000378:metabolism*; D007249:Inflammation / Q000517:prevention & control; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D051379:Mice; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D009822:Oils, Volatile / Q000494:pharmacology*
D008070:Lipopolysaccharides; D009822:Oils, Volatile; D009569:Nitric Oxide; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D020929:Mitogen-Activated Protein Kinase Kinases; D015232:Dinoprostone