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J Physiol Pharmacol. 2011 Apr;62(2):229-38.

Trans fatty acids induce a proinflammatory response in endothelial cells through ROS-dependent nuclear factor-κB activation.

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Department of Biochemistry and Clinical Chemistry, The Warsaw Medical University, Warsaw, Poland.


It has been shown that increased intake of trans fatty acids (TFAs) is associated with a higher risk of cardiovascular disease. In this study, we have investigated the effects of linoelaidic (LA) and elaidic (EA) acids on the proinflammatory response in endothelial cells, a key step in vascular disease. Human aortic endothelial cells (HAECs) were treated with different concentrations (100 μmol/l in most experiments) of LA or EA for different periods of time. The surface protein and mRNA expression of ICAM-1 and VCAM-1 were determined by flow cytometry and real time RT-PCR, respectively. Adhesion of leukocytes to TFA-treated HAECs was evaluated by an adhesion assay. Activation of nuclear factor-κB (NF-κB) was evaluated by measuring NF-κB p65 phosphorylation using flow cytometry. ROS production was determined by the reduction of fluorescent 2',7'-dichlorofluorescein diacetate (DCFH-DA). LA treatment significantly increased protein and mRNA levels of ICAM-1 and VCAM-1, leukocyte adhesion to HAECs, phosphorylation of NF-κB and ROS generation. Similar effects were achieved for cells incubated with EA. Experiments with HAECs pretreated with pyrrolidine dithiocarbamate, an inhibitor of NF-κB, revealed that both LA and EA-mediated induction of ICAM-1 and VCAM-1 is mainly regulated by NF-κB. The ROS production induced by both of the studied acids was inhibited in the presence of diphenyleneiodonium (DPI), a NADPH oxidase inhibitor, suggesting ROS production through the activation of NADPH oxidase. Furthermore, LA or EA-induced ICAM-1 and VCAM-1 expression, activation of NF-κB and adhesion of leukocytes to HAECs were abolished in the presence of DPI.


TFAs present in our diet have a direct proinflammatory effect, which promotes leukocyte adhesion to the endothelium through ROS-dependent NF-κB activation.

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