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The Essential Oil Isolated from Artemisia capillaris Prevents LPS-Induced Production of NO and PGE2 by Inhibiting MAPK-Mediated Pathways in RAW 264.7 Macrophages
Authors:Jeong-Dan Cha  Sang-Eun Moon  Hye-Young Kim  Jeong-Chae Lee
Affiliation:1. Oral Cancer Research Institute, College of Dentistry, Yonsei University, Seoul, Korea;2. Department of Oral Microbiology and Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea;3. Department of Dental Hygiene, Dongeul University, Busan, South Korea;4. Laboratory of Cell Biology in Department of Orthodontics and Institute of Oral Bioscience, Chonbuk National University, Jeonju, Korea;5. Research Center of Bioactive Materials, Chonbuk National University, Jeonju, Korea
Abstract: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 E2 (PGE2). 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 PGE2 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 IκB-α, nuclear translocation of p65, and subsequent activation of NF-κB. 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 PGE2. 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-κB and AP-1.
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