title: Lysimachia clethroides Duby extract attenuates inflammatory response in Raw 264.7 macrophages stimulated with lipopolysaccharide and in acute lung injury mouse model.
abstract: BACKGROUND
  Lysimachia clethroides Duby (LC) is a traditional medicinal herb used to treat edema, hepatitis and inflammatory diseases in China and other Asian countries. In this study, the anti-inflammatory effects of LC extract and the mechanisms underlying were explored in both in vitro cell lines and acute lung injury (ALI) animal model of inflammation in vivo.
  
  
  METHODS
  Lipopolysaccharide (LPS)-stimulated Raw 264.7 murine macrophages were used to study the regulatory effects of LC extract on inflammatory mediators such as nitric oxide (NO) and proinflammatory cytokine expression. Western blotting or ELISA techniques were employed to estimate protein levels. RT-PCR was used for analyzing the interferon (IFN)-β production. LPS-induced ALI mouse model in vivo was employed to study the effect of LC extract. Further high-performance liquid chromatography (HPLC) fingerprinting technique was used to evaluate the active constituents present in LC extract, compared with reference standards.
  
  
  RESULTS
  Pre-treatment with LC extract inhibited the LPS-stimulated NO release, interleukin (IL)-1β and IL-6 production in Raw 264.7 cells dose dependently. LC extract inhibited the LPS-stimulated IRF3 and STAT1 phosphorylation. Further, in vivo experiments revealed that LC extract suppressed the infiltration of immune cells into the lung and proinflammatory cytokine production in broncho-alveolar lavage fluid (BALF) in the LPS-induced ALI mouse model.
  
  
  CONCLUSIONS
  Our results indicate that LC extract attenuates LPS-stimulated inflammatory responses in macrophages via regulating the key inflammatory mechanisms, providing a scientific support for its traditional use in treating various inflammatory diseases.
authors.affiliation: Department of Biotechnology, College of Biomedical and Health Science, Research Institute of Inflammatory Diseases, Konkuk University, Chungju 380-701, Republic of Korea.
authors.forename: Do-Wan
authors.initials: DW
authors.lastname: Shim
authors.forename: Ji-Won
authors.initials: JW
authors.lastname: Han
authors.forename: Xiao
authors.initials: X
authors.lastname: Sun
authors.forename: Cheol-Hun
authors.initials: CH
authors.lastname: Jang
authors.forename: Sushruta
authors.initials: S
authors.lastname: Koppula
authors.forename: Tack-Joong
authors.initials: TJ
authors.lastname: Kim
authors.forename: Tae-Bong
authors.initials: TB
authors.lastname: Kang
authors.forename: Kwang-Ho
authors.initials: KH
authors.lastname: Lee
mesh_terms: D055371:Acute Lung Injury / Q000188:drug therapy* / Q000276:immunology / Q000473:pathology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002460:Cell Line; D016207:Cytokines / Q000276:immunology; D005260:Female; D050838:Interferon Regulatory Factor-3 / Q000276:immunology; D008070:Lipopolysaccharides; D008168:Lung / Q000187:drug effects / Q000276:immunology / Q000473:pathology; D008264:Macrophages; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology; D009569:Nitric Oxide / Q000276:immunology; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D029623:Primulaceae; D050794:STAT1 Transcription Factor / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D050838:Interferon Regulatory Factor-3; C494233:Irf3 protein, mouse; D008070:Lipopolysaccharides; D010936:Plant Extracts; D050794:STAT1 Transcription Factor; C494080:Stat1 protein, mouse; D009569:Nitric Oxide
keywords: Acute lung injury; Inflammation; Interleukin; Lipopolysaccharide; Lysimachia clethroides; TRIF