title: β-Carotene and lycopene affect endothelial response to TNF-α reducing nitro-oxidative stress and interaction with monocytes.
abstract: METHODS
  Cardiovascular disease (CVD) is associated with vascular oxidative imbalance and inflammation. Increased reactive oxygen species (ROS) generation is associated with a functional inactivation of nitric oxide (NO) due to the reaction with O₂⁻, leading to peroxynitrite (ONOO⁻) formation and subsequent reduction in the beneficial effect of vascular NO bioavailability. Carotenoids'-rich diets have been associated with decreased risk of CVD, but the underlying mechanism is still unknown.
  
  
  RESULTS
  In human umbilical vein endothelial cells (HUVECs), both β-carotene (BC) or lycopene (Lyc) significantly affected tumor necrosis factor-α (TNF-α)-induced inflammation, being associated with a significant decrease in the generation of ROS (spectrofluorometry) and nitrotyrosine (an index of ONOO⁻ formation, cytofluorimetry), an increased NO/cGMP (cyclic guanosine monophosphate) levels (EIA), and a down-regulation of NF-κB-dependent adhesion molecule expression (Western blot and EMSA) and monocyte-HUVEC interaction (adhesion assay). Our results indicate that BC or Lyc treatment reduce the inflammatory response in TNF-α-treated HUVECs. This is due to the redox balance protection and to the maintenance of NO bioavailability.
  
  
  CONCLUSIONS
  Our observations provide background for a novel mechanism for carotenoids' anti-inflammatory activity in the vasculature and may contribute to a better understanding of the protective effects of carotenoid-rich diets against CVD risk.
authors.affiliation: Department of Biomedical Sciences, "G. d'Annunzio" University, Chieti-Pescara, Italy.
authors.forename: Pamela
authors.initials: P
authors.lastname: Di Tomo
authors.forename: Raffaella
authors.initials: R
authors.lastname: Canali
authors.forename: Domenico
authors.initials: D
authors.lastname: Ciavardelli
authors.forename: Sara
authors.initials: S
authors.lastname: Di Silvestre
authors.forename: Alessandro
authors.initials: A
authors.lastname: De Marco
authors.forename: Annalisa
authors.initials: A
authors.lastname: Giardinelli
authors.forename: Caterina
authors.initials: C
authors.lastname: Pipino
authors.forename: Natalia
authors.initials: N
authors.lastname: Di Pietro
authors.forename: Fabio
authors.initials: F
authors.lastname: Virgili
authors.forename: Assunta
authors.initials: A
authors.lastname: Pandolfi
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D001682:Biological Availability; D002338:Carotenoids / Q000493:pharmacokinetics / Q000494:pharmacology*; D002448:Cell Adhesion / Q000187:drug effects; D015815:Cell Adhesion Molecules / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism; D000077276:Lycopene; D009000:Monocytes / Q000166:cytology / Q000187:drug effects*; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism* / Q000494:pharmacology; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism; D019207:beta Carotene / Q000493:pharmacokinetics / Q000494:pharmacology*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D015815:Cell Adhesion Molecules; D016328:NF-kappa B; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D019207:beta Carotene; D009569:Nitric Oxide; D002338:Carotenoids; C002744:3-nitrotyrosine; D014443:Tyrosine; D006152:Cyclic GMP; D000077276:Lycopene