Sodium casein-derived peptides modulate the expression of pro-inflammatory phenotype of EC via PPAR-γ dependent mechanisms. TNF-α (0.5 ng/ml, 6 h) induced VCAM-1, ICAM-1 and E-sel expression was blocked by the PPAR-γ ligand, troglitazone (25 μM), similarly to the casein hydrolysate (300 300 μg/ml). In the presence of GW9662 (10 μM), a PPAR-γ antagonist, the effects of both troglitazone and the casein hydrolysate were completely reversed. (A) Gene expression levels of VCAM-1, ICAM-1 and E-sel were measured in EC treated with casein hydrolysate or troglitazone for 18 h and with or without GW9662 (10 μM), followed by 6 h stimulation with TNF-α (0.5 ng/ml). (B) Quantification of protein surface expression of adhesion molecules was carried out by flow cytometric analysis. Data are expressed as mean ± SEM of 3 independent experiments. Data were reported as percentage of control (TNF-α activated EC). Statistical comparison of one condition versus control was made by using Student’s unpaired t-test assuming unequal variance; $$$ (p < 0.001) vehicle vs. control; **P < 0.01 and *P < 0.05 treatment vs. control; ##P < 0.01 and #P < 0.05 treatment vs. GW9662.