title: Carpesium macrocephalum attenuates lipopolysaccharide-induced inflammation in macrophages by regulating the NF-κB/IκB-α, Akt, and STAT signaling pathways.
abstract: Carpesium macrocephalum (CM) Fr. et Sav. (Compositae) has been used in Chinese folk medicine as an analgesic, hemostatic, antipyretic, and to suppress inflammatory conditions. In the present study we aimed to provide scientific evidence for the anti-inflammatory properties of CM extract and evaluate the intrinsic mechanisms involved in both in vitro and in vivo experimental models. In in vitro findings, CM significantly inhibited the LPS-stimulated release of proinflammatory mediators such as nitric oxide, tumor necrosis factor-alpha, prostaglandin E2, and interleukin-6 in RAW264.7 macrophages in a concentration-dependent fashion. The attenuation of inflammatory responses in LPS-activated RAW264.7 cells by CM was closely associated with the suppression of nuclear factor-kappa B (NF-κB) phosphorylation, IκB-α degradation, and phosphorylation of Akt. CM treatment also attenuated the phosphorylation of STAT through TRIF dependent pathways in LPS-activated RAW264.7 cells. In vivo studies revealed that CM extract concentration dependently suppressed the acetic acid-induced vascular permeability in mice. Considering the data obtained regulation of multiple signaling mechanisms involving TRIF and Akt/NF-κB pathways might be responsible for the potent anti-inflammatory action of CM, substantiating its traditional use in inflammatory diseases.
authors.affiliation: Department of Biotechnology, College of Biomedical and Health Science, Research Institute of Inflammatory Diseases, Konkuk University, Chungju 380-701, Korea.
authors.forename: Sushruta
authors.initials: S
authors.lastname: Koppula
authors.forename: Wan-Jae
authors.initials: WJ
authors.lastname: Kim
authors.forename: Jun
authors.initials: J
authors.lastname: Jiang
authors.forename: Do-Wan
authors.initials: DW
authors.lastname: Shim
authors.forename: Na-Hyun
authors.initials: NH
authors.lastname: Oh
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: D000818:Animals; D019659:Asteraceae; D002199:Capillary Permeability / Q000187:drug effects*; D015232:Dinoprostone / Q000276:immunology; D004731:Endotoxins / Q000276:immunology / Q000633:toxicity; D020672:I-kappa B Proteins / Q000187:drug effects / Q000378:metabolism; D015850:Interleukin-6 / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology / Q000633:toxicity; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology; D051379:Mice; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000187:drug effects / Q000378:metabolism; D009569:Nitric Oxide; D010936:Plant Extracts / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000187:drug effects / Q000378:metabolism; D050791:STAT Transcription Factors / Q000187:drug effects / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects* / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000276:immunology
chemical_list: D004731:Endotoxins; D020672:I-kappa B Proteins; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D010936:Plant Extracts; D050791:STAT Transcription Factors; D014409:Tumor Necrosis Factor-alpha; D000072000:NF-KappaB Inhibitor alpha; D009569:Nitric Oxide; D051057:Proto-Oncogene Proteins c-akt; D015232:Dinoprostone