title: Phenolic-rich fraction from Rhus verniciflua Stokes (RVS) suppress inflammatory response via NF-kappaB and JNK pathway in lipopolysaccharide-induced RAW 264.7 macrophages.
abstract: The effects of phenolic-rich fraction (PRF) from Rhus verniciflua Stokes (Anacardiaceae) on the activities of cellular signaling molecules that mediate inflammatory responses in LPS-induced RAW 264.7 macrophages were investigated. At various concentrations of PRF significantly inhibited NO, PGE(2) and TNF-alpha production in LPS-induced RAW 264.7 macrophage cells. The PRF also significantly inhibited iNOS and COX-2 protein expression in LPS-induced RAW 264.7 macrophage in a concentration-dependent manner. Transcription factor NF-kappaB plays a key role for the inducible expression of genes mediating proinflammatory effects and here, we show that PRF can inhibit the induction of NF-kappaB activity. The PRF effectively inhibited the iNOS and COX-2 protein expression through suppression of phospho-JNK1/2 activation. Study using PDA HPLC has found that the PRF contains several low molecular compounds (i.e. p-coumaric acid, fustin, kaempferol-3-O-glucoside, sulfuretin, butein, kaempferol). Our results indicate that the anti-inflammatory properties of PRF might result from the inhibition of pro-inflammatory mediators (e.g., NO, PGE(2) and TNF-alpha) by suppression of such signaling pathways as NF-kappaB and JNK1/2.
authors.affiliation: Laboratory of Clinical Biology and Pharmacogenomics, College of Oriental Medicine, Kyunghee University, Seoul 130-701, Republic of Korea.
authors.forename: Chang Hwa
authors.initials: CH
authors.lastname: Jung
authors.forename: Ji Hye
authors.initials: JH
authors.lastname: Kim
authors.forename: Myung Hee
authors.initials: MH
authors.lastname: Hong
authors.forename: Ho Moon
authors.initials: HM
authors.lastname: Seog
authors.forename: Seong Hoon
authors.initials: SH
authors.lastname: Oh
authors.forename: Pan Jae
authors.initials: PJ
authors.lastname: Lee
authors.forename: Gyung Jun
authors.initials: GJ
authors.lastname: Kim
authors.forename: Hyung Min
authors.initials: HM
authors.lastname: Kim
authors.forename: Jae Young
authors.initials: JY
authors.lastname: Um
authors.forename: Seong-Gyu
authors.initials: SG
authors.lastname: Ko
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage / Q000737:chemistry / Q000494:pharmacology*; D002460:Cell Line; D002470:Cell Survival; D051546:Cyclooxygenase 2 / Q000187:drug effects; D015232:Dinoprostone / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects; D048031:JNK Mitogen-Activated Protein Kinases / Q000187:drug effects* / Q000378:metabolism; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000187:drug effects* / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000187:drug effects; D010636:Phenols / Q000008:administration & dosage / Q000302:isolation & purification / Q000494:pharmacology*; D008517:Phytotherapy; D024301:Plant Bark; D010936:Plant Extracts / Q000737:chemistry / Q000494:pharmacology; D010946:Plants, Medicinal; D029045:Rhus / Q000737:chemistry*; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010636:Phenols; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D048031:JNK Mitogen-Activated Protein Kinases; D015232:Dinoprostone