Dairy fat intake has been considered as a risk factor for
cardiovascular disease. Rodent models show that
trans fatty acids in industrial hydrogenated oil and ruminant milk have different effects on
cardiovascular diseases. One of the main reasons is that the distributions of
trans fatty acids in
triacylglycerols from dairy products and from industrial hydrogenated oil are different, which affects
lipid absorption and metabolism. This study investigated the effects of 1,3-olein-2-elaidin (OEO, representing industrial hydrogenated oil
triacylglycerols) and 1-vaccenic-2,3-olein (OOV, representing ruminant
triacylglycerols in dairy products) on the function of human umbilical vein endothelial cells (HUVEC), including cell viability,
lactate dehydrogenase (LDH) exudation rate, and
nitric oxide secretory and
nitric oxide synthase relative activity. We found that the detrimental effect of OEO on HUVEC was significantly greater than that of OOV. The results also showed that the absorption rate of OEO in HUVEC (78.25%) was significantly greater than that of OOV (63.32%). Mechanistically, based on phospholipidomics analysis, we found that
calcium-independent phospholipase A2 (iPLA2) played a key role with regard to the OOV-mediated
arachidonic acid (ARA)/COX-2/PG pathway, whereas
secretory phospholipase A2 (
sPLA2) and cytoplasmic
phospholipase A2 (cPLA2) are responsible for the OEO-mediated ARA/COX-2/PG pathway. Moreover, OEO had a greater effect on the
protein expression of COX-2 and PG secretion than OOV. In addition, iPLA2,
sPLA2, and cPLA2 could mediate the ARA/CYP4A11 pathway in OOV-treated HUVEC, but only iPLA2 could mediate this pathway in HUVEC treated with OEO. We also found that
sPLA2 could mediate the ARA/5-LOX pathway in HUVEC treated with OOV, but none of these 3 forms of PLA2 could mediate this pathway in HUVEC treated with OEO. On the other hand, after OOV treatment, trans-11 C18:1 was converted to beneficial forms of
fatty acids in HUVEC, including
conjugated linoleic acid (CLA) and trans-9 C16:1. In conclusion, we elucidated the potential mechanisms that might account for the diverse effects of
triacylglycerols from industrial hydrogenated oil and ruminant milk on the function of HUVEC.