Eicosapentaenoic acid significantly suppressed palmitic acid-induced increases in the expression of adhesion molecules, cytokines, and inflammatory proteins in human umbilical vein endothelial cells.
Does eicosapentaenoic acid prevent palmitic acid-induced vascular endothelial dysfunction in human umbilical vein endothelial cells?
EPA prevents saturated fatty acid-induced vascular endothelial dysfunction in vitro by regulating ACSL3 expression and downstream inflammatory pathways.
valor p: p=<0.05
AIM: Vascular endothelial dysfunction is considered an early predictor of atherosclerosis. It has been proven that elevated blood levels of free fatty acids pose a substantial risk for the development of cardiovascular disease. In this study, we examined the effects of palmitic acid (PA), a saturated fatty acid, on endothelial function by using the expression of adhesion molecule, cytokines, and inflammatory protein as indicators, as well as investigated the effects of eicosapentaenoic acid, an n-3 polyunsaturated fatty acid. METHODS: Human umbilical vein endothelial cells (HUVEC) were exposed to PA and EPA. RESULTS: When HUVEC were exposed to PA, there was an increase in the expression of adhesion molecule, cytokines, and inflammatory protein (ICAM-1, MCP-1, interleukin-6, PTX3). PA augmented the expression of long-chain acyl-CoA synthetase (ACSL) and the cyclin-dependent kinase inhibitor p21, and enhanced the phosphorylation of p65, a component of NF-κB. ACSL inhibition and siRNA-mediated ACSL3 knockdown suppressed the PA-induced increase in the expression of adhesion molecule, cytokines, and inflammatory protein, and ACSL inhibition suppressed the enhancement of p65 phosphorylation. In addition, p21 knockdown suppressed the PA-induced increase in the expression of MCP-1 and ICAM-1. EPA suppressed the PA-induced increase in the expression of ACSL and p21, the enhancement of p65 phosphorylation, as well as the associated increase in the expression of ICAM-1, MCP-1, interleukin-6, and PTX3. CONCLUSIONS: These results suggest that the ACSL, p21, and NF-κB-dependent pathway may possibly be involved in PA-induced vascular endothelial dysfunction, and that EPA ameliorates this at least in part through the regulation of ACSL3 expression.
Ishida et al. (Thu,) conducted a other in Vascular endothelial dysfunction. Eicosapentaenoic acid (EPA) vs. Palmitic acid (PA) alone or vehicle was evaluated on Expression and secretion of adhesion molecules, cytokines, and inflammatory proteins (ICAM-1, MCP-1, IL-6, PTX3) (p=<0.05). Eicosapentaenoic acid significantly suppressed palmitic acid-induced increases in the expression of adhesion molecules, cytokines, and inflammatory proteins in human umbilical vein endothelial cells.