Palmitoleic Acid has Stronger Anti‐Inflammatory Potential in Human Endothelial Cells Compared to Oleic and Palmitic Acids

<jats:sec><jats:title>Scope</jats:title><jats:p>Fatty acids (FAs) may affect endothelial cell (EC) function, influencing atherogenesis and inflammatory processes. Palmitoleic acid (POA) has been described as an anti‐inflammatory FA. However, its effects on ECs are underexplored. This study compares the effects of POA with those of palmitic acid (PA) and oleic acid (OA) on EC inflammatory responses.</jats:p></jats:sec><jats:sec><jats:title>Methods and Results</jats:title><jats:p>EAHy926 cells (EC lineage) are exposed to PA, OA, or POA, and stimulated with tumor necrosis factor (TNF)‐α. Associated with the FA's own incorporation, PA induces a twofold increase in arachidonic acid, while POA increases the amount of cis‐vaccenic acid. PA, but not OA, enhances the production of IL‐6 and IL‐8 in response to TNF‐α. In contrast, POA decreases production of monocyte chemotactic protein (MCP)‐1, IL‐6, and IL‐8 compared to PA. TNF‐α increases surface intercellular adhesion molecule‐1 expression previously decreased by POA. TNF‐α stimulation increases the expression of NFκB, cyclooxygenase (COX)‐2, MCP‐1, and IL‐6 genes and reduces the expression of peroxisome proliferator‐activated receptor (PPAR)‐α gene. PA enhances the expression of MCP‐1, IL‐6, and COX‐2 genes, while POA downregulates these genes, decreases expression of NFκB, and upregulates PPAR‐α gene expression.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>POA has anti‐inflammatory effects on ECs stimulated with TNF‐α and may counter endothelial dysfunction.</jats:p></jats:sec>