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J Nutr Biochem. 2014 Aug;25(8):824-33. doi: 10.1016/j.jnutbio.2014.03.011. Epub 2014 Apr 4.

Sulforaphane reduces vascular inflammation in mice and prevents TNF-α-induced monocyte adhesion to primary endothelial cells through interfering with the NF-κB pathway.

Author information

1
Department of Biology, The University of North Carolina at Greensboro, Greensboro, NC 27412, USA.
2
Department of Family and Consumer Sciences, College of Agriculture, Human and Natural Sciences, Tennessee State University, Nashville, TN 37209, USA.
3
Division of Nutrition, College of Health, University of Utah, Salt Lake City, UT 84112, USA.
4
Department of Gene and Cell Engineering, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing 100193, PR China.
5
Departments of Human Nutrition, Foods and Exercise, College of Agriculture and Life Sciences, Virginia Tech, Blacksburg, VA 24062, USA.
6
Department of Pharmacology, School of Osteopathic Medicine, Campbell University, Buies Creek, NC 27506, USA.
7
Departments of Human Nutrition, Foods and Exercise, College of Agriculture and Life Sciences, Virginia Tech, Blacksburg, VA 24062, USA. Electronic address: doliu@vt.edu.
8
Department of Pharmacology, School of Osteopathic Medicine, Campbell University, Buies Creek, NC 27506, USA. Electronic address: yli@campbell.edu.
9
Department of Biology, The University of North Carolina at Greensboro, Greensboro, NC 27412, USA. Electronic address: z_jia@uncg.edu.

Abstract

Sulforaphane, a naturally occurring isothiocyanate present in cruciferous vegetables, has received wide attention for its potential to improve vascular function in vitro. However, its effect in vivo and the molecular mechanism of sulforaphane at physiological concentrations remain unclear. Here, we report that a sulforaphane concentration as low as 0.5 μM significantly inhibited tumor necrosis factor-α (TNF-α)-induced adhesion of monocytes to human umbilical vein endothelial cells, a key event in the pathogenesis of atherosclerosis both in static and under flow conditions. Such physiological concentrations of sulforaphane also significantly suppressed TNF-α-induced production of monocyte chemotactic protein-1 and adhesion molecules including soluble vascular adhesion molecule-1 and soluble E-selectin, key mediators in the regulation of enhanced endothelial cell-monocyte interaction. Furthermore, sulforaphane inhibited TNF-α-induced nuclear factor (NF)-κB transcriptional activity, Inhibitor of NF-κB alpha (IκBα) degradation and subsequent NF-κB p65 nuclear translocation in endothelial cells, suggesting that sulforaphane can inhibit inflammation by suppressing NF-κB signaling. In an animal study, sulforaphane (300 ppm) in a mouse diet significantly abolished TNF-α-increased ex vivo monocyte adhesion and circulating adhesion molecules and chemokines in C57BL/6 mice. Histology showed that sulforaphane treatment significantly prevented the eruption of endothelial lining in the intima layer of the aorta and preserved elastin fibers' delicate organization, as shown by Verhoeff-van Gieson staining. Immunohistochemistry studies showed that sulforaphane treatment also reduced vascular adhesion molecule-1 and monocyte-derived F4/80-positive macrophages in the aorta of TNF-α-treated mice. In conclusion, sulforaphane at physiological concentrations protects against TNF-α-induced vascular endothelial inflammation, in both in vitro and in vivo models. This anti-inflammatory effect of sulforaphane may be, at least in part, associated with interfering with the NF-κB pathway.

KEYWORDS:

In vivo; Physiological concentrations; Sulforaphane; TNF-α; Vascular inflammation

PMID:
24880493
PMCID:
PMC4087147
DOI:
10.1016/j.jnutbio.2014.03.011
[Indexed for MEDLINE]
Free PMC Article

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