title: Inhibition of endothelial adhesion molecule expression by Monascus purpureus-fermented rice metabolites, monacolin K, ankaflavin, and monascin.
abstract: BACKGROUND
  Inflammation is an independent risk factor of cardiovascular diseases and is associated with endothelial dysfunction. Monascus purpureus-fermented rice, containing naturally occurring statins and various pigments, has lipid-modulating, anti-inflammatory and antioxidative effects.
  
  
  RESULTS
  The effects of monacolin K, ankaflavin and monascin, as metabolites from Monascus-fermented rice, on the expression of cell adhesion molecules (intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecular-1 (VCAM-1) and E-selectin) by tumor necrosis factor (TNF)-α-treated human aortic endothelial cells (HAECs) were investigated. Supplement of HAECs with these Monascus-fermented rice metabolites significantly suppressed cellular binding between the human monocytic cells U937 and TNF-α-stimulated HAECs. Immunoblot analysis showed that Monascus-fermented rice metabolites significantly attenuated TNF-α-induced VCAM-1 and E-selectin but not ICAM-1 protein expression. Gel shift assays showed that Monascus-fermented rice metabolites treatment reduced TNF-α-activated transcription factor nuclear factor (NF)-κB. Furthermore, Monascus-fermented rice metabolites also attenuated reactive oxygen species (ROS) generation in vitro and in TNF-α-treated HAECs. Supplement with an ROS scavenger N-acetylcysteine gave similar results as compared with Monascus-fermented rice metabolites.
  
  
  CONCLUSIONS
  Monascus-fermented rice metabolites reduced TNF-α-stimulated endothelial adhesiveness as well as downregulating intracellular ROS formation, NF-κB activation, and VCAM-1/E-selectin expression in HAECs, supporting the notion that the various metabolites from Monascus-fermented rice might have potential implications in clinical atherosclerosis disease.
authors: Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. cplin@vghtpe.gov.tw
authors: Chih-Pei
authors: CP
authors: Lin
authors: Yun-Lian
authors: YL
authors: Lin
authors: Po-Hsun
authors: PH
authors: Huang
authors: Hui-Szu
authors: HS
authors: Tsai
authors: Yung-Hsiang
authors: YH
authors: Chen
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D001011:Aorta / Q000166:cytology; D002448:Cell Adhesion / Q000187:drug effects; D002460:Cell Line; D019040:E-Selectin / Q000378:metabolism; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism; D005285:Fermentation; D005415:Flavins / Q000494:pharmacology*; D006575:Heterocyclic Compounds, 3-Ring / Q000494:pharmacology*; D006801:Humans; D008148:Lovastatin / Q000494:pharmacology*; D032741:Monascus; D016328:NF-kappa B / Q000378:metabolism; D012275:Oryza / Q000378:metabolism* / Q000382:microbiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism*
chemical_list: D019040:E-Selectin; D005415:Flavins; D006575:Heterocyclic Compounds, 3-Ring; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; C499916:ankaflavin; D008148:Lovastatin; C517880:monascin; D000111:Acetylcysteine