State Key Laboratory of Food Science and Technology, Institute for Advanced Study, Nanchang University , Nanchang, Jiangxi 330047, P.R. China.
J Agric Food Chem. 2014 Jan 22;62(3):798-807. doi: 10.1021/jf404834e. Epub 2014 Jan 8.
Our previous study showed that trans-fatty acids can cause apoptosis of endothelial cells through the caspase pathway and the mitochondrial pathway. The objective of this study was to explore how trans-fatty acids activate the caspase pathway, whether there exist specific receptors induced apoptosis by comparing normal cells and non-rafts cells treated with elaidic acid (9t18:1) and oleic acid (9c18:1), respectively. Compared to normal cells treated with 9t18:1, the cell viability increased by 13% and the number of apoptotic cells decreased by 3% in non-rafts cells treated with 9t18:1 (p < 0.05), and the expression levels of pro-apoptotic proteins such as caspase-3, -8, -9, Bax, and Bid decreased, and expression of antiapoptotic protein Bcl-2 increased (p < 0.05). In addition, Fas/FasL expression in cell membrane decreased significantly (p < 0.05). In conclusion, the lipid rafts and Fas/FasL pathway may involve in 9t18:1-induced apoptosis of human umbilical vein endothelial cells.
我们之前的研究表明，反式脂肪酸可通过半胱氨酸天冬氨酸蛋白酶（caspase）途径和线粒体途径引起血管内皮细胞凋亡。本研究旨在探讨反式脂肪酸如何通过 caspase 途径激活，以及是否存在特定的受体通过比较正常细胞和未形成脂筏的细胞分别用反油酸（9t18:1）和油酸（9c18:1）处理后诱导细胞凋亡。与用 9t18:1 处理的正常细胞相比，用 9t18:1 处理的非脂筏细胞的细胞活力增加了 13%，凋亡细胞的数量减少了 3%（p<0.05），并且促凋亡蛋白如 caspase-3、-8、-9、Bax 和 Bid 的表达水平降低，抗凋亡蛋白 Bcl-2 的表达水平升高（p<0.05）。此外，细胞膜上 Fas/FasL 的表达明显降低（p<0.05）。总之，脂筏和 Fas/FasL 途径可能参与了 9t18:1 诱导的人脐静脉内皮细胞凋亡。
