title: The roots of Nardostachys jatamansi inhibits lipopolysaccharide-induced endotoxin shock.
abstract: Nardostachys jatamansi (NJ) has been used in the treatment of inflammatory diseases. However, it is not clear how NJ produces anti-inflammatory effects. In the present study, using an experimental model of lipopolysaccharide (LPS)-induced endotoxin shock, the protective effects and mechanisms of action of NJ were investigated. The water extract of roots of NJ was administrated to mice orally (1, 5, and 10 mg/kg) 1 h after or before LPS challenge. The administration of NJ inhibited LPS-induced endotoxin shock and the production of inflammatory mediators, such as interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and interferon (IFN)-α/β. Murine peritoneal macrophages were used to determine the production of inflammatory mediators. In peritoneal macrophages, NJ also inhibited LPS-induced production of inflammatory mediators, such as IL-1β, IL-6, TNF-α, and IFN-α/β. In addition, NJ reduced the activation of mitogen-activated protein kinases (MAPKs) and the level of expression of interferon regulatory factor (IRF)-1 and IRF-7 mRNA. Furthermore, post-treatment with NJ reduced LPS-induced endotoxin shock and the production of inflammatory mediators. These results suggest that NJ inhibits endotoxin shock by inhibiting the production of IL-1β, IL-6, TNF-α, and IFN-α/β through the inhibition of MAPKs activation and IRF induction.
authors.affiliation: Department of Herbology, School of Oriental Medicine, Wonkwang University, Iksan, Jeonbuk 540-749, South Korea.
authors.forename: Gi-Sang
authors.initials: GS
authors.lastname: Bae
authors.forename: Sang-Wan
authors.initials: SW
authors.lastname: Seo
authors.forename: Min-Sun
authors.initials: MS
authors.lastname: Kim
authors.forename: Kyoung-Chel
authors.initials: KC
authors.lastname: Park
authors.forename: Bon Soon
authors.initials: BS
authors.lastname: Koo
authors.forename: Won-Seok
authors.initials: WS
authors.lastname: Jung
authors.forename: Gil-Hwan
authors.initials: GH
authors.lastname: Cho
authors.forename: Hyun Cheol
authors.initials: HC
authors.lastname: Oh
authors.forename: Seung-Won
authors.initials: SW
authors.lastname: Yun
authors.forename: Jong-Jin
authors.initials: JJ
authors.lastname: Kim
authors.forename: Sung Gyu
authors.initials: SG
authors.lastname: Kim
authors.forename: Sung-Yeon
authors.initials: SY
authors.lastname: Hwang
authors.forename: Ho-Joon
authors.initials: HJ
authors.lastname: Song
authors.forename: Sung-Joo
authors.initials: SJ
authors.lastname: Park
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002478:Cells, Cultured; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D053583:Interleukin-1beta / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity*; D051379:Mice; D008810:Mice, Inbred C57BL; D032404:Nardostachys / Q000737:chemistry*; D010936:Plant Extracts / Q000737:chemistry* / Q000627:therapeutic use*; D018517:Plant Roots / Q000737:chemistry*; D012772:Shock, Septic / Q000188:drug therapy*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha
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