Dietary curcumin inhibits atherosclerosis by affecting the expression of genes involved in leukocyte adhesion and transendothelial migration
Article first published online: 2 JUL 2012
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 56, Issue 8, pages 1270–1281, August 2012
How to Cite
Coban, D., Milenkovic, D., Chanet, A., Khallou-Laschet, J., Sabbe, L., Palagani, A., Vanden Berghe, W., Mazur, A. and Morand, C. (2012), Dietary curcumin inhibits atherosclerosis by affecting the expression of genes involved in leukocyte adhesion and transendothelial migration. Mol. Nutr. Food Res., 56: 1270–1281. doi: 10.1002/mnfr.201100818
- Issue published online: 10 AUG 2012
- Article first published online: 2 JUL 2012
- Manuscript Accepted: 12 MAY 2012
- Manuscript Revised: 10 MAY 2012
- Manuscript Received: 16 DEC 2011
- Macrophage infiltration;
- Monocyte adhesion;
The aim of the study was to examine the atheroprotective effect of dietary curcumin in a mouse model of atherosclerosis and to identify its cellular and molecular targets at the vascular level.
Methods and results
ApoE–/– mice were fed with curcumin at 0.2% (wt/wt) in diet for 4 months. This supplementation reduced the extent of atherosclerotic lesion by 26% and induced changes in expression of genes implicated in cell adhesion and transendothelial migration or cytoskeleton organization, as revealed by a transcriptomic analysis in the aorta. Expression profile of these genes suggests reduction in both leukocyte adhesion and transendothelial migration. In agreement with this hypothesis, we observed a reduction (–37%) in macrophage infiltration in the plaque, as measured by immunohistochemistry, and, in vitro, a lower adhesion of monocytes to TNF-α-stimulated endothelial cells (–32%) after exposure to a nutritionally achievable concentration of curcumin. These changes in gene expression could be related to the observed increased expression of IκB protein and decrease of TNF-α-induced NF-κB/DNA binding and NF-κB-transcriptional activity upon exposure to curcumin.
Our findings pointed out that the antiatherogenic effect of curcumin could be linked to its effect on gene networks and cell functions related to leukocyte adhesion and transendothelial migration via NF-κB-dependent pathways.