title: Cocoa consumption reduces NF-κB activation in peripheral blood mononuclear cells in humans.
abstract: OBJECTIVE
  Epidemiological studies have demonstrated an association between high-polyphenol intake and reduced incidence of atherosclerosis. The healthy effects of cocoa-polyphenols may be due to their antioxidant and anti-inflammatory actions, although the exact mechanisms are unknown and depend on the matrix in which cocoa-polyphenols are delivered. Nuclear factor κB (NF-κB) is a key molecule in the pathophysiology of atherosclerosis involved in the regulation of adhesion molecules(AM) and cytokine expression and its activation is the first step in triggering the inflammatory process. The aim of this study was to evaluate the effect of acute cocoa consumption in different matrices related to the bioavailability of cocoa-polyphenols in NF-κB activation and the expression of AM.
  
  
  RESULTS
  Eighteen healthy volunteers randomly received 3 interventions: 40g of cocoa powder with milk (CM), with water (CW), and only milk (M). NF-κB activation in leukocytes and AM (sICAM, sVCAM, E-selectin) were measured before and 6h after each intervention. Consumption of CW significantly decreased NF-κB activation compared to baseline and to CM (P < 0.05, both), did not change after CM intervention, and significantly increased after M intervention (P = 0.014). sICAM-1 concentrations significantly decreased after 6h of CW and CM interventions (P ≤ 0.026; both) and E-selectin only decreased after CW intervention (P = 0.028). No significant changes were observed in sVCAM-1 concentrations.
  
  
  CONCLUSIONS
  The anti-inflammatory effect of cocoa intake may depend on the bioavailability of bioactive compounds and may be mediated at least in part by the modulation of NF-κB activation and downstream molecules reinforcing the link between cocoa intake and health.
authors.affiliation: Department of Internal Medicine, Hospital Clinic, Villarroel 170, 08036 Barcelona, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Vázquez-Agell
authors.forename: M
authors.initials: M
authors.lastname: Urpi-Sarda
authors.forename: E
authors.initials: E
authors.lastname: Sacanella
authors.forename: S
authors.initials: S
authors.lastname: Camino-López
authors.forename: G
authors.initials: G
authors.lastname: Chiva-Blanch
authors.forename: V
authors.initials: V
authors.lastname: Llorente-Cortés
authors.forename: E
authors.initials: E
authors.lastname: Tobias
authors.forename: E
authors.initials: E
authors.lastname: Roura
authors.forename: C
authors.initials: C
authors.lastname: Andres-Lacueva
authors.forename: R M
authors.initials: RM
authors.lastname: Lamuela-Raventós
authors.forename: L
authors.initials: L
authors.lastname: Badimon
authors.forename: R
authors.initials: R
authors.lastname: Estruch
mesh_terms: D000328:Adult; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000975:Antioxidants / Q000494:pharmacology; D001628:Beverages; D001682:Biological Availability; D015153:Blotting, Western; D002099:Cacao / Q000737:chemistry*; D015815:Cell Adhesion Molecules; D018592:Cross-Over Studies; D019040:E-Selectin / Q000235:genetics / Q000378:metabolism; D005260:Female; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000187:drug effects*; D008297:Male; D008875:Middle Aged; D008892:Milk; D016328:NF-kappa B; D059808:Polyphenols / Q000008:administration & dosage / Q000493:pharmacokinetics; D011446:Prospective Studies; D015398:Signal Transduction; D014157:Transcription Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D015815:Cell Adhesion Molecules; D019040:E-Selectin; C573420:ICAM1 protein, human; D016328:NF-kappa B; D059808:Polyphenols; D014157:Transcription Factors; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1