title: Natural flavone kaempferol suppresses chemokines expression in human monocyte THP-1 cells through MAPK pathways.
abstract: There is increasing evidence that daily intake of flavonoids reduced severity and prevalence of allergic diseases. However, the mechanism of its antiinflammatory effects in allergic diseases remains uncertain. Kaempferol, which belongs to the flavone group, is a strong antioxidant among natural flavonoids and is the essential component of many beverages and vegetables. Because chemokine is one of the key mediators in allergic inflammatory process, we investigated the effect of kaempferol on chemokines expression in monocytes. Our data demonstrated that kaempferol significantly inhibited the lipopolysaccharide (LPS)-induced production of monocyte-derived chemokine (MDC), interferon gamma-induced protein 10 (IP-10), and interleukin-8 (IL-8) in THP-1 cells. Growth-related oncogene-α (GRO-α) was also suppressed at a higher concentration. We also found that kaempferol was able to suppress LPS-induced mitogen-activated protein kinase (MAPK) pathways, as well as the phosphorylation of upstream c-raf and MEK1/2. In brief, kaempferol suppressed LPS-induced T helper 1 (Th1), T helper 2 (Th2), and neutrophil-related chemokines production in monocytes might be via the MAPK pathways.
authors.affiliation: Dept. of Pediatrics, Yuan's General Hospital, Taiwan.
authors.forename: Ching-Hua
authors.initials: CH
authors.lastname: Huang
authors.forename: Ren-Long
authors.initials: RL
authors.lastname: Jan
authors.forename: Chang-Hung
authors.initials: CH
authors.lastname: Kuo
authors.forename: Yu-Te
authors.initials: YT
authors.lastname: Chu
authors.forename: Wei-Li
authors.initials: WL
authors.lastname: Wang
authors.forename: Min-Sheng
authors.initials: MS
authors.lastname: Lee
authors.forename: Huan-Nan
authors.initials: HN
authors.lastname: Chen
authors.forename: Chih-Hsing
authors.initials: CH
authors.lastname: Hung
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D002460:Cell Line; D054422:Chemokine CCL22 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism*; D019743:Chemokines, CXC / Q000378:metabolism; D015536:Down-Regulation / Q000187:drug effects*; D006801:Humans; D006967:Hypersensitivity / Q000517:prevention & control; D016209:Interleukin-8 / Q000378:metabolism; D044949:Kaempferols / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000633:toxicity; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D009000:Monocytes / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D009994:Osmolar Concentration; D010766:Phosphorylation / Q000187:drug effects; D020033:Protein Isoforms / Q000378:metabolism; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; C515482:CCL22 protein, human; C508606:CXCL8 protein, human; D054422:Chemokine CCL22; D018925:Chemokines; D019743:Chemokines, CXC; D016209:Interleukin-8; D044949:Kaempferols; D008070:Lipopolysaccharides; D020033:Protein Isoforms; D047428:Protein Kinase Inhibitors; C006552:kaempferol; D048051:p38 Mitogen-Activated Protein Kinases