2. Academic Validation
  3. 9c11tCLA modulates 11t18:1 and 9t18:1 induced inflammations differently in human umbilical vein endothelial cells

9c11tCLA modulates 11t18:1 and 9t18:1 induced inflammations differently in human umbilical vein endothelial cells

  • Sci Rep. 2018 Jan 24;8(1):1535. doi: 10.1038/s41598-018-19729-9.
Jing Li 1,  Sheng-Ben Hu 1,  Yue-Ming He 1,  Cheng-Fei Zhuo 1,  Ruo-Lin Zhou 1,  Fang Chen 1,  Hong-Yan Li 1,  Ze-Yuan Deng 2 3
Affiliations

Affiliations

  • 1 State Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China.
  • 2 State Key Lab of Food Science and Technology, Nanchang University, Nanchang, 330047, China. [email protected].
  • 3 Institute for Advanced Study, Nanchang University, Nanchang, 330031, China. [email protected].
PMID: 29367652 DOI: 10.1038/s41598-018-19729-9
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.

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