title: Anti-inflammatory activity and molecular mechanism of Oolong tea theasinensin.
abstract: Oolong tea theasinensins are a group of tea polyphenols different from green tea catechins and black tea theaflavins, and they are considered as bioactive compounds in Oolong tea. In the present study, based on the properties of theasinensin and information about inflammatory processes, we investigated the anti-inflammatory activity and molecular mechanisms of theasinensin A (TSA) in both cell and animal models. In the cell model, TSA reduced the levels of pro-inflammatory mediators including inducible nitric oxide synthase (iNOS), nitric oxide (NO), interleukin-12 (IL-12) (p70), tumor necrosis factor alpha (TNF-α), and monocyte chemotactic protein-1 (MCP-1) induced by lipopolysaccharide (LPS). Cellular signaling analysis revealed that TSA downregulated MAPK/ERK kinase (MEK)-extracellular signal-regulated kinase (ERK) signaling. Pull-down assay and affinity data revealed that TSA might directly bind to MEK-ERK for the inhibitory action. In the animal model, TSA suppressed the production of IL-12 (p70), TNF-α, and MCP-1 and attenuated mouse paw edema induced by LPS.
authors.affiliation: United Graduate School of Agricultural Science, Faculty of Agriculture, Kagoshima University, Korimoto 1-21-24, Kagoshima, 890-0065, Japan. hou@chem.agri.kagoshima-u.ac.jp.
authors.forename: Ayami
authors.initials: A
authors.lastname: Hisanaga
authors.forename: Hisako
authors.initials: H
authors.lastname: Ishida
authors.forename: Kozue
authors.initials: K
authors.lastname: Sakao
authors.forename: Takayuki
authors.initials: T
authors.lastname: Sogo
authors.forename: Takuma
authors.initials: T
authors.lastname: Kumamoto
authors.forename: Fumio
authors.initials: F
authors.lastname: Hashimoto
authors.forename: De-Xing
authors.initials: DX
authors.lastname: Hou
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001578:Benzopyrans / Q000494:pharmacology*; D045744:Cell Line, Tumor; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D004195:Disease Models, Animal; D015536:Down-Regulation; D004487:Edema / Q000139:chemically induced / Q000188:drug therapy; D018664:Interleukin-12 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000009:adverse effects; D048369:MAP Kinase Kinase 1 / Q000235:genetics / Q000378:metabolism; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D010636:Phenols / Q000494:pharmacology*; D028321:Plant Preparations / Q000494:pharmacology*; D013662:Tea / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D001578:Benzopyrans; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D008070:Lipopolysaccharides; D010636:Phenols; D028321:Plant Preparations; D013662:Tea; D014409:Tumor Necrosis Factor-alpha; C481298:theasinensin A; D018664:Interleukin-12; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D048369:MAP Kinase Kinase 1; C482127:Map2k1 protein, mouse