Abstract
Endothelial inflammation is recognized as the initial stage of a multistep process leading to coronary heart disease (CHD). Recently, the different effects of industrial trans fatty acids (elaidic acid, 9t18:1) and ruminant trans fatty acids (vaccenic acid, 11t18:1) on CHD have been reported in epidemiological and animal studies, however, the mechanism was not fully studied. Therefore, the objective of this study was to explore the underlying mechanism by which 9t18:1 and 11t18:1 affect human umbilical vein endothelial cells (HUVECs) inflammation. We found that 9c11t-CLA modulated the inflammation of HUVECs induced by 9t18:1 and 11t18:1. Fatty acid composition, pro-inflammatory factors, phosphorylation of MAPKs, and the TLR4 level in HUVECs altered by 11t18:1 induction, collectively suggest that the bio-conversion of 11t18:1 to 9c11tCLA might be the cause why 11t18:1 and 9t18:1 have distinct influences on endothelial injuries. It was concluded that it is biosynthesis of 9c11t CLA from11t18:1, and the modulation of TLR4-MAPK pathway by 9c11t CLA, which at least partially account for the slight effect of 11t18:1 on endothelial inflammation.
Highlights
Dietary trans fatty acids (TFA) have acquired an unsavory reputation for a long time due to its strong correlation with coronary heart disease (CHD)
Leptin was reported to down-regulate the mRNA and protein expression of SCD-1, leptin was used to inhibit the bio-conversion of 11t 18:1 into 9c11t CLA in this study
Compared with the control group, the mRNA and protein expression of SCD-1 was reduced when human umbilical vein endothelial cells (HUVECs) was treated with leptin (Fig. 1)
Summary
Dietary trans fatty acids (TFA) have acquired an unsavory reputation for a long time due to its strong correlation with coronary heart disease (CHD). Most epidemiological studies suggested an inverse or no association between R-TFA intake and CHD across multiple geographical locations[5,6,7,8]. Animal studies showed R-TFA intake is positively correlated with CHD. Another study[13] pointed that ruminant consumption resulted in an increase of many other trans isomers of 18:1 than VA, and many conjugated fatty acids in addition to rumenic acid, which were potential risk factors for CHD. Other animal studies suggested that R-TFA had a beneficial effect on CHD. Many studies reported that TFA could induce endothelial cell dysfunction and inflammation, which are integral components of the development and progression of CHD22. Our previous studies observed that endothelial cell injuries induced by VA were significantly weaker than that by EA25. Several animal studies had reported the beneficial effects of CLA intake on atherosclerotic lesions and CVD26–28. The aim of this study was to explore the occurrence of bio-conversion from VA to 9c11t-CLA, and to evaluate the influence of this bio-conversion on cell dysfunctions mediated by VA and EA
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