4B). The treatment with OA at 300 μM decreased the lipids content by 56% compared to vehicle. The association of OA with PUFA (ω-3 and ω-6) increased the NL content compared to OA at 300 μM by: 30% and 25% for EPA and γA, respectively, selleck inhibitor both at 50 μM and 37% for LA at 100 μM (Fig. 4C). OA associated with ω-3 and ω-6 PUFA did not alter the ROS production compared

to OA (Fig. 4D). FFA are important mediators of endothelial dysfunction, atherosclerosis and cardiovascular disease (Azekoshi et al., 2010). In this study, SA increased the EC death and ROS production, without affecting NL content. ω-3 PUFA did not protect EC from death induced by SA but increased the lipids content and decreased the ROS production. In contrast, ω-6 PUFA reduced cell death induced by SA, increased lipids accumulation and decreased ROS content. SA-induced cell death confirms the results obtained in previous studies (Artwohl et al., 2004 and Rioux and Legrand, 2007. Artwohl et al., 2008 showed that SA causes apoptosis of various EC lines selleck (HUVECs, HAECs, and EPCs HRECs). Saturated FA (stearic and palmitic acid) are the most abundant FFA in plasma (Hagenfeldt et al., 1972) and the major components of parenteral and enteral nutritional formulations, so the potential for adverse vascular effects initiated by saturated FA are cause for clinical concern. EC apoptosis plays an important role in endothelium

dysfunction and directly affects blood thrombogenicity through

the release of apoptotic microparticles into the bloodstream (Blann et al., 2009). ω-3 PUFA have important anti-inflammatory and anti-apoptotic properties (Massaro et al., 2008 and Suphioglu et al., 2010). Artwohl et al. (2008) showed that low EPA levels (5–20 μM) inhibits SA-induced apoptosis in HUVEC, HAEC, EPC and HREC. In our study, EPA increased the percentage of viable cells without affecting DNA fragmentation Endonuclease induced by SA. However a marked decrease in the proportion of cells with death signs was found in the treatment with ω-6 PUFA and SA. No significant association between LA (ω-6 PUFA) intake (or tissues levels) and CHD risk (Esrey et al., 1996 and Pietinen et al., 1997) and no consistent relations between stroke and LA intake (He et al., 2002 and Sauvaget et al., 2004) have been found. Herein, ω-6 PUFA protected EC from death induced by SA. SA did not affect EC NL content, but it does so in association of SA with ω-3 or ω-6 PUFA. Thus, PUFA, specially ω-6, may protect from SA-induced EC death by incorporating FA into NL (Cnop et al., 2001). ROS have been implicated in the initiation and progression of atherosclerosis. ROS can oxidize lipoproteins, limit the vascular availability of antiatherosclerotic NO, and promote vascular expression of cytokines and adhesion molecules. Treatment of ECV-304 cells with SA for 30 min led to an increase of ROS.