Erythorbyl laurate suppresses TNF-α-induced adhesion of monocytes to the vascular endothelium

Abstract

Erythorbyl laurate (EL) can be produced via lipase-catalyzed esterification between erythorbic acid and lauric acid. In this study, we evaluate the anti-inflammatory effect of EL in the early stage of atherosclerosis. EL suppressed tumor necrosis factor (TNF)-α-induced monocyte adhesion to vascular endothelial cells and expression of vascular cell adhesion molecule (VCAM)-1 in human umbilical vein endothelial cells (HUVECs). Additionally, EL suppressed TNF-α-induced p65/IκB kinase (IKK)/IκB phosphorylation in HUVECs. Western blot analysis of cytosolic and nuclear cell fractions and immunofluorescence showed that EL suppressed TNF-α-induced translocation of p65 from the cytoplasm to the nucleus. EL also inhibited phosphorylation of extracellular-signal-regulated kinase (ERK) 1/2, p38, and c-Jun N-terminal kinases (JNK) 1/2 in HUVECs. EL suppressed TNF-α-induced phosphorylation of Akt, IRAK1, and TAK1 in HUVECs. Quantitative RT-PCR analysis showed that EL significantly suppressed TNF-α-induced interleukin (IL)1B, IL6, TNFA, and CCL2 mRNA expression in HUVECs. Additionally, oral administration of EL suppressed TNF-α-induced IL6 and TNFA expression in the mouse aorta. EL could represent a promising functional nutrient that can be ingested for the prevention of vascular inflammation via decreased monocyte infiltration to the vascular endothelium and suppression of inflammatory nuclear factor (NF)-κB and mitogen-activated protein kinases (MAPKs) signaling pathways.

Keywords

• Erythorbyl laurate
• Arteriosclerosis
• Monocyte adhesion
• Vascular inflammation
• VCAM-1
• NF-κB