title: Vitamin C suppresses lipopolysaccharide-induced procoagulant response of human monocyte-derived macrophages.
abstract: Although vitamin C is a strong antioxidant, the epidemiologic evidence to support its role in lowering risk of cardiovascular disease is inconsistent. In order to define the role of vitamin C in vascular pathophysiology, we have investigated the effect of vitamin C on the tissue factor (TF) and Factor VII Activating Protease (FSAP) expression induced by lipopolysaccharide (LPS) in human monocyte-derived macrophages.
  
  
  
  Vitamin C at clinically relevant doses was tested to its ability to influence the LPS- and reactive oxygen species (ROS) - generating system of xanthine/xanthine oxidase (X/XO) NF-kB activity in human monocyte-derived macrophages.
  
  
  
  Vitamin C-treatment prevents LPS- and ROS-induced DNA-binding activity of NF-kB in a concentration-dependent fashion. Vitamin C also inhibited the phosphorylation and proteolytic degradation of the inhibitor protein IkBa. In parallel to regulate NF-kB activity, vitamin C reduced the expression of TF and FSAP, genes known to be induced by bacterial LPS and triggered the extrinsic coagulation cascade and linked thrombosis with inflammation.
  
  
  
  Vitamin C alters pro-inflammatory and pro-coagulatory processes via inhibition of NF-kB activation and exerts beneficial antiatherogenic effects on human monocyte-derived macrophages in addition to its anti-oxidant properties.
authors.affiliation: Internal Medicine/Cardiology and Angiology, University Hospital of Giessen and Marburg, Giessen, Germany. mariana.parahuleva@innere.med.uni-giessen.de.
authors.forename: M S
authors.initials: MS
authors.lastname: Parahuleva
authors.forename: J
authors.initials: J
authors.lastname: Jung
authors.forename: M
authors.initials: M
authors.lastname: Burgazli
authors.forename: A
authors.initials: A
authors.lastname: Erdogan
authors.forename: B
authors.initials: B
authors.lastname: Parviz
authors.forename: H
authors.initials: H
authors.lastname: Hölschermann
mesh_terms: D001205:Ascorbic Acid / Q000494:pharmacology*; D001777:Blood Coagulation / Q000187:drug effects*; D006801:Humans; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects* / Q000502:physiology; D016328:NF-kappa B / Q000378:metabolism; D012697:Serine Endopeptidases / Q000378:metabolism; D013925:Thromboplastin / Q000378:metabolism
chemical_list: D008070:Lipopolysaccharides; D016328:NF-kappa B; D013925:Thromboplastin; C433550:HABP2 protein, human; D012697:Serine Endopeptidases; D001205:Ascorbic Acid