화학공학소재연구정보센터
Biochemical and Biophysical Research Communications, Vol.387, No.4, 633-640, 2009
Nitrated fatty acids prevent TNF alpha-stimulated inflammatory and atherogenic responses in endothelial cells
Nitration products (nitroalkenes) of linoleic acid (LNO2) and oleic acid (OA-NO2) can act as endogenous PPAR gamma ligands with electrophilic properties to exert anti-inflammatory effects on atherosclerotic plaques in the vasculature. Here, we show that OA-NO2 and LNO2 prevent tumor necrosis factor alpha (TNF alpha)-stimulated inflammatory and atherogenic responses in human umbilical vein endothelial cells (HUVECs). Both OA-NO2 and LNO2 prevented TNF alpha-stimulated release of the cytokines, IL-6, IL-8, IL-12/p40, IFN gamma, MCP-1, and IP-10, and inhibited NF-kappa B activation. OA-NO2 and LNO2 also blocked TNF alpha-induced expression of the adhesion molecules, ICAM-1, VCAM-1, and E-selectin, and suppressed monocyte adhesion to HUVECs. In each case, OA-NO2 was more potent and efficacious than was LNO2, possibly due to increased stability in aqueous media. Collectively, these results substantiate a new functional role for nitrated fatty acids, demonstrating that OA-NO2 and LNO2 exert an anti-inflammatory function against the inflammatory cascade initiated by the representative pro-inflammatory cytokine, TNF alpha. (C) 2009 Elsevier Inc. All rights reserved.