De-alcoholised white and red wines decrease inflammatory markers and NF-κB in atheroma plaques in apoE-deficient mice.
OBJECTIVE
Wine polyphenols attenuate the development of atherosclerosis, which involves an inflammatory process. We studied the beneficial effect of de-alcoholised white and red wines (DWW and DRW, respectively) on the development of atheroma plaques and on the expression of biomarkers.


METHODS
We administered control or de-alcoholised wine-rich diets to apoE-deficient mice for 12 or 20 weeks. We then used optical microscopy or immunofluorescence to examine atherosclerotic lesion development in the thoracic aorta and aortic root and assessed the presence of cytokines and adhesion molecules by qPCR and immunofluorescence in total aorta and aortic root, respectively.


RESULTS
Atherosclerotic lesions in thoracic aorta were significantly decreased in mice supplemented with DWW (30 %) and DRW (62 %) for 20 weeks. In addition, the expressions of interferon-γ, interleukin-1β, the monocyte chemoattractant protein-1 and CD68 were reduced by DRW. The adhesion molecule P-selectin, vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 were decreased by 52, 76 and 45 %, respectively, in mice fed DRW for 12 weeks, whereas DWW reduced these parameters in a minor extent. The NF-κB expression in total aorta was significantly decreased in the mice treated with de-alcoholised wines for 12 weeks.


CONCLUSIONS
DRW is shown to be more effective than DWW on cytokines and adhesion molecule expression, in the early stages of the inflammatory events associated with atherosclerosis development, probably due to the high phenolic content of red wine. Downregulation of NF-κB expression may be involved in the mechanism by which de-alcoholised wines modulate atherosclerosis.
Departament de Fisiologia i Immunologia, Facultat de Biologia, IRNSA, Universitat de Barcelona, Barcelona, Spain.
Nuria
N
Martínez
Kelly
K
Casós
Paolo
P
Simonetti
María P
MP
Sáiz
Juan J
JJ
Moreno
María T
MT
Mitjavila
D000818:Animals; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000235:genetics / Q000378:metabolism; D001013:Aorta, Thoracic / Q000187:drug effects / Q000473:pathology; D001057:Apolipoproteins E / Q000172:deficiency*; D015415:Biomarkers / Q000097:blood*; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism; D015536:Down-Regulation; D000431:Ethanol / Q000302:isolation & purification*; D005455:Fluorescent Antibody Technique; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism*; D019007:P-Selectin / Q000235:genetics / Q000378:metabolism; D058226:Plaque, Atherosclerotic / Q000378:metabolism* / Q000473:pathology; D059808:Polyphenols / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D014920:Wine / Q000032:analysis*; D000097382:CD68 Molecule
D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D001057:Apolipoproteins E; D015415:Biomarkers; D018932:Chemokine CCL2; D000431:Ethanol; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma; D053583:Interleukin-1beta; D016328:NF-kappa B; D019007:P-Selectin; D059808:Polyphenols; D019010:Vascular Cell Adhesion Molecule-1; C081026:CD68 protein, mouse; D000097382:CD68 Molecule; C491768:Ccl2 protein, mouse