Quercetin protects against linoleic acid-induced porcine endothelial cell dysfunction.

Consumption of plant phenolics, such as quercetin, may be associated with decreased risk of cardiovascular disease by stabilizing and protecting vascular endothelial cells against oxidative and proinflammatory insults. The present study focused on the effect of quercetin on linoleic acid-induced oxidative stress and the inflammatory pathways of nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1). Because the transcription factor peroxisome proliferator activated receptor gamma (PPARgamma) was reported to downregulate inflammatory pathways, we further investigated the effect of quercetin on PPARgamma. Porcine pulmonary-arterial endothelial cells were activated with linoleic acid in the presence or absence of quercetin. Oxidative stress was markedly induced by endothelial cell exposure to linoleic acid and diminished by treatment with quercetin as measured via the oxidation of 2',7'-dichlorofluorescin. Quercetin reduced linoleic acid-mediated binding activity of NF-kappaB and AP-1 and mRNA levels of inflammatory genes such as interleukin-6 (IL-6) and vascular cell adhesion molecule-1 (VCAM-1). Cotreatment of linoleic acid plus quercetin or vitamin E also decreased linoleic acid-induced binding activity of PPARgamma. These data suggest that quercetin has potent antioxidative and anti-inflammatory properties and protects endothelial cells against linoleic acid-mediated cell dysfunction.