title: The n-butanol fraction of Naematoloma sublateritium suppresses the inflammatory             response through downregulation of NF-κB in human endothelial cells.
abstract: Naematoloma sublateritium (Fr.) P. Karst is a chestnut mushroom that is             currently a popular edible fungus in the USA, Japan, China and Korea. Although             its therapeutic potential in the treatment of diseases has been demonstrated,             the pharmacological effect of N. sublateritium (NS) has been poorly studied. In             the present study, we demonstrate for the first time that NS suppresses TNF-α-induced             inflammatory response in human umbilical vein endothelial cells. The n-butanol             fraction of NS (BFNS) inhibited TNF-α-induced monocyte adhesion to endothelial             cells in a dose-dependent manner. The anti-adhesive activity of BFNS correlated             with suppressed expression of vascular cell adhesion molecule-1, intercellular             adhesion molecule-1, monocyte chemoattractant protein-1 and interleukin-8 at both             the mRNA and protein levels. In addition, BFNS dose-dependently decreased the             expression of inducible nitrogen oxygen synthase (iNOS) and cyclooxygenase-2 (COX-2).             Notably, BFNS significantly regulated the nuclear factor (NF)-κB transcriptional             activity that was activated by TNF-α stimulation. When considered together, these             results suggest that BFNS inhibits the expression of TNF-α-induced adhesion molecules             in addition to regulating the iNOS/COX-2 pathways through the modulation of NF-κB             in endothelial cells. In conclusion, we propose that BFNS may be a potential therapeutic             agent against vascular inflammation, such as atherosclerosis.
authors.affiliation: Department of Physiology, School of Medicine, Chungnam National                     University, Daejeon 301747, Republic of Korea.
authors.forename: Yu Ran
authors.initials: YR
authors.lastname: Lee
authors.forename: Ki Mo
authors.initials: KM
authors.lastname: Kim
authors.forename: Byeong Hwa
authors.initials: BH
authors.lastname: Jeon
authors.forename: Jong Woon
authors.initials: JW
authors.lastname: Choi
authors.forename: Sunga
authors.initials: S
authors.lastname: Choi
mesh_terms: D020001:1-Butanol / Q000737:chemistry; D000363:Agaricales / Q000737:chemistry*; D000893:Anti-Inflammatory Agents / Q000302:isolation & purification* / Q000494:pharmacology*; D002448:Cell Adhesion / Q000187:drug effects; D018932:Chemokine CCL2 / Q000235:genetics; D015536:Down-Regulation / Q000187:drug effects*; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics; D016209:Interleukin-8 / Q000235:genetics; D009000:Monocytes / Q000166:cytology; D016328:NF-kappa B / Q000235:genetics* / Q000276:immunology; D012333:RNA, Messenger / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D018932:Chemokine CCL2; D016209:Interleukin-8; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D020001:1-Butanol