Trans fatty acids influence the oxidation of LDL in ECV304 cells

Abstract

The objectives of this study are to explore whether separate sources of trans fatty acids (TFA) have different effects on ECV304 cell line and to further elucidate the oxidation mechanism induced by TFA. ECV304 cells are used in the study because they display many endothelial features. Cell apoptosis rates increased in a dose-dependent manner following 24-h treatment with TFA from separate sources. Additionally, TFA stimulated human alpha-defensin 1 (HNP-1) expression and resulted in a significant increase in both malondialdehyde (MDA) and ROS levels. MDA levels reach their peak at 18 h. HNP-1 expression levels increase at 2 h and then reach their peak at 10 h. At the same time, the protein carbonyl (PCO) value declines slightly. After 10 h of TFA co-culture, the cells were washed and fresh low-density lipoprotein (LDL) was added. MDA generation significantly increased after 6 h and it could be inhibited by 4-aminobenzoic acid hydrazide (ABAH) or sodium ferulate. However, after the TFA co-culture for 2 h, adding LDL for 6 h just caused slight MDA generation change and the MDA generation could be inhibited by verapamil or sodium ferulate. TFA from different sources did not have different effects on ECV304. HNP-1 mediates the oxidation induced by TFA by activating ROS. Furthermore, TFA can stimulate the oxidation of LDL in ECV304 cells through both passive and active pathway. In the oxidation induced by linoelaidic acid, ABAH can decrease the MDA generation in active oxidation pathway and verapamil can decrease the MDA generation in passive oxidation pathway.