title: Red wine intake prevents nuclear factor-kappaB activation in peripheral blood mononuclear cells of healthy volunteers during postprandial lipemia.
abstract: BACKGROUND
  Several epidemiological studies have demonstrated the beneficial effect of red wine intake in reducing total and cardiovascular mortality. This effect has been attributed in part to its antioxidant properties. Because the monocytes/macrophages and the nuclear transcription factor kappaB (NF-kappaB) are implicated in the pathogenesis of atherosclerotic lesions, we examined the effect of red wine intake on the activation of NF-kappaB in peripheral blood mononuclear cells.
  
  
  RESULTS
  Sixteen healthy volunteers were studied 3 times each: after a moderate dose, a low dose, and no wine with a fat-enriched breakfast. Lipid profile and NF-kappaB activation (electrophoretic mobility shift assay) were examined in blood samples taken before and 3, 6, and 9 hours after wine intake. In addition, mononuclear cells were incubated with VLDL in the presence of some antioxidants (quercetin and alpha-tocopherol succinate) contained in red wine to study their effects on NF-kappaB activation. Subjects receiving a fat-enriched breakfast had increased NF-kappaB activation in peripheral blood mononuclear cells coinciding with the augmentation in total triglycerides and chylomicrons. Red wine intake prevented NF-kappaB activity even though it induced a certain increase in serum lipids, particularly VLDL, that did not increase after the fat ingestion alone. However, another form of alcohol intake (vodka) did not modify the NF-kappaB activation provided by postprandial lipemia. In cultured mononuclear cells, isolated human VLDL caused NF-kappaB activation in a time-dependent manner that did not occur in the presence of the red wine antioxidants quercetin and alpha-tocopherol.
  
  
  CONCLUSIONS
  Our results provide a new potential mechanism to explain the beneficial effects of red wine intake in the reduction of cardiovascular mortality.
authors.affiliation: Research Laboratory, Instituto de Investigación Médica, Fundación Jiménez Díaz, Universidad Autónoma de Madrid, Spain.
authors.forename: L M
authors.initials: LM
authors.lastname: Blanco-Colio
authors.forename: M
authors.initials: M
authors.lastname: Valderrama
authors.forename: L A
authors.initials: LA
authors.lastname: Alvarez-Sala
authors.forename: C
authors.initials: C
authors.lastname: Bustos
authors.forename: M
authors.initials: M
authors.lastname: Ortego
authors.forename: M A
authors.initials: MA
authors.lastname: Hernández-Presa
authors.forename: P
authors.initials: P
authors.lastname: Cancelas
authors.forename: J
authors.initials: J
authors.lastname: Gómez-Gerique
authors.forename: J
authors.initials: J
authors.lastname: Millán
authors.forename: J
authors.initials: J
authors.lastname: Egido
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000032:analysis / Q000494:pharmacology*; D001161:Arteriosclerosis / Q000517:prevention & control; D002460:Cell Line; D004041:Dietary Fats / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008079:Lipoproteins, VLDL / Q000037:antagonists & inhibitors / Q000097:blood / Q000494:pharmacology; D008297:Male; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism*; D019518:Postprandial Period; D011794:Quercetin / Q000494:pharmacology; D013997:Time Factors; D014280:Triglycerides / Q000097:blood; D014810:Vitamin E / Q000494:pharmacology; D014920:Wine / Q000032:analysis
chemical_list: D000975:Antioxidants; D004041:Dietary Fats; D008055:Lipids; D008079:Lipoproteins, VLDL; D016328:NF-kappa B; D014280:Triglycerides; D014810:Vitamin E; D011794:Quercetin