Sargachromenol protects against vascular inflammation by preventing TNF-α-induced monocyte adhesion to primary endothelial cells via inhibition of NF-κB activation

Vascular inflammation is a key factor in the pathogenesis of atherosclerosis. The purpose of this study was to investigate the protective effects of sargachromenol (SCM) against tumor necrosis factor (TNF)-alpha-induced vascular inflammation. SCM decreased the expression of cell adhesion molecules, including intracellular adhesion molecule-1 and vascular cell adhesion molecule-1, in TNF-alpha-stimulated human umbilical vein endothelial cells (HUVECs), resulted in reduced adhesion of monocytes to HUVECs. SCM also decreased the production of monocyte chemoattractant protein-1 and matrix metalloproteinase-9 in TNF-alpha-induced HUVECs. Additionally, SCM inhibited activation of nuclear factor kappa B (NF-kappa B) induced by TNF-alpha through preventing the degradation of inhibitor kappa B. Moreover, SCM reduced the production of reactive oxygen species in TNF-alpha-treated HUVECs. Overall, SCM alleviated vascular inflammation through the regulation of NF-kappa B activation and through its intrinsic antioxidant activity in TNF-alpha-induced HUVECs. These results indicate that SCM may have potential application as a therapeutic agent against vascular inflammation. (C) 2016 Elsevier B.V. All rights reserved.