title: Inhibitory effect of Coptis chinensis on inflammation in LPS-induced endotoxemia.
abstract: BACKGROUND
  Rhizoma coptidis (RC) has been used as a remedy for inflammation-related diseases in traditional medicine. Although it is known to have anti-inflammatory activities, its mechanism of action on lipopolysaccharide (LPS)-induced inflammation has not yet been identified in detail.
  
  
  OBJECTIVE
  This study was designed to assess the beneficial effects of pretreatment with RC in ameliorating LPS-induced liver inflammation.
  
  
  METHODS
  Mice were orally administered RC (500, 1000 mg/kg) for three days in a row. 1h after the last RC administration, the mice were intraperitoneally injected with LPS (35 mg/kg). After treatment, histological alterations and inflammatory factor levels in the liver and proinflammatory cytokines in the serum associated with inflammation were examined.
  
  
  RESULTS
  We found that pretreatment with RC (500 and 1000 mg/kg) exerted a significant protective effect by attenuating liver histopathological changes in endotoxemic mice. The results also demonstrated that RC suppressed secretion of LPS-stimulated pro-inflammatory cytokines, such as interleukin-6 (IL-6). Furthermore, RC inhibited LPS-mediated nuclear factor (NF)-κB activation via the prevention of IκB-α phosphorylation, as well as the phosphorylation of ERK1/2, JNK, and p38 MAPKs. These results were associated with decreases in the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (I-NOS).
  
  
  CONCLUSIONS
  The results presented here clearly demonstrate that RC could significantly protect mice against LPS-induced acute liver injury.
authors.affiliation: Department of Prescriptionology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.
authors.forename: You Yeon
authors.initials: YY
authors.lastname: Choi
authors.forename: Mi Hye
authors.initials: MH
authors.lastname: Kim
authors.forename: Ik-Hyun
authors.initials: IH
authors.lastname: Cho
authors.forename: Ji Hee
authors.initials: JH
authors.lastname: Kim
authors.forename: Jongki
authors.initials: J
authors.lastname: Hong
authors.forename: Tae Hee
authors.initials: TH
authors.lastname: Lee
authors.forename: Woong Mo
authors.initials: WM
authors.lastname: Yang
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D039323:Coptis; D051546:Cyclooxygenase 2 / Q000378:metabolism; D019446:Endotoxemia / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005260:Female; D006505:Hepatitis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D020672:I-kappa B Proteins / Q000378:metabolism; D007371:Interferon-gamma / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008070:Lipopolysaccharides; D008099:Liver / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D051379:Mice; D008813:Mice, Inbred ICR; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D027343:Rhizome
chemical_list: D000893:Anti-Inflammatory Agents; D020672:I-kappa B Proteins; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D000072000:NF-KappaB Inhibitor alpha; D007371:Interferon-gamma; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; C077623:Ptgs2 protein, mouse; D051546:Cyclooxygenase 2; D020928:Mitogen-Activated Protein Kinases
keywords: Coptis chinensis; IL-6; Lipopolysaccharide (LPS); MAPKs; NF-κB