title: Salicortin suppresses lipopolysaccharide-stimulated inflammatory responses via blockade of NF-κB and JNK activation in RAW 264.7 macrophages.
abstract: We isolated the phenolic glucoside salicortin from a Populus euramericana bark extract, and examined its ability to suppress inflammatory responses as well as the molecular mechanisms underlying these abilities, using lipopolysaccharide (LPS)-stimulated RAW264.7 cells. Salicortin inhibited iNOS expression and the subsequent production of NO in a dose-dependent manner in the LPS-stimulated RAW 264.7 cells. Salicortin significantly suppressed LPS-induced signal cascades of NF-κB activation, such as IKK activation, IκBα phosphorylation and p65 phosphorylation in RAW 264.7 cells. In addition, salicortin inhibited the LPS-induced activation of JNK, but not ERK or p38 MAPK. Furthermore, salicortin significantly inhibited production of pro-inflammatory cytokines, such as TNF-α, IL-1β and IL-6 in the LPS-stimulated RAW 264.7 cells. These findings suggest that salicortin may show its anti-inflammatory activity by suppressing the LPS-induced expression of pro-inflammatory mediators through inhibition of NF-κB and JNK MAPK signaling cascades in macrophages.
authors.affiliation: Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702; Hongcheon Institute of Medicinal Herb, Hongcheon 200-930, Korea.
authors.forename: Dong-Joo
authors.initials: DJ
authors.lastname: Kwon
authors.affiliation: Department of Forest Biomaterials Engineering, Kangwon National University, Chuncheon 200-701, Korea.
authors.forename: Young-Soo
authors.initials: YS
authors.lastname: Bae
authors.affiliation: Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Korea.
authors.forename: Sung Mi
authors.initials: SM
authors.lastname: Ju
authors.affiliation: Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Korea.
authors.forename: Gi Soo
authors.initials: GS
authors.lastname: Youn
authors.affiliation: Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Korea.
authors.forename: Soo Young
authors.initials: SY
authors.lastname: Choi
authors.affiliation: Department of Biomedical Science and Research Institute for Bioscience & Biotechnology, Hallym University, Chuncheon 200-702, Korea.
authors.forename: Jinseu
authors.initials: J
authors.lastname: Park
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D016207:Cytokines / Q000378:metabolism; D005960:Glucosides / Q000494:pharmacology*; D020672:I-kappa B Proteins / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000633:toxicity; D008264:Macrophages / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D024301:Plant Bark / Q000378:metabolism; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology; D032107:Populus / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; D005960:Glucosides; D020672:I-kappa B Proteins; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D010936:Plant Extracts; D051996:Transcription Factor RelA; D000072000:NF-KappaB Inhibitor alpha; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D048031:JNK Mitogen-Activated Protein Kinases; C113068:salicortin