AimTo investigate the molecular mechanism of inflammatory protein expression via transforming growth factor-β1 (TGF-β1)/Smad pathway in ox-LDL-stimulated human umbilical vein endothelial cells (HUVEC).MethodsHUVEC were treated with 0.1 g/L of ox-LDL.TGF-β1, Smad3, VCAM-1 and ICAM-1 protein expression, and Smad3 phosphorylation were detemined by Western blot.Resultsox-LDL obviously increased the expression of VCAM-1 and ICAM-1 in HUVEC.TGF-β1 expression and Smad3 phosphorylation were enhanced in ox-LDL-stimulated HUVEC.Nuclear extract analysis showed that the phosphorylated Smad3 expression was increased in ox-LDL-treated cells.SIS3 (a specific inhibitor of Smad3) inhibited Smad3 phosphorylation in a dose-dependent manner, however, VCAM-1 and ICAM-1 expression were increased in ox-LDL-treated cells.ConclusionsTGF-β1/Smad signaling involved in the regulation of inflammatory protein expression in HUVEC induced by ox-LDL, the inhibition of Smad3 phosphorylation increased the expression of inflammatory protein, suggesting that TGF-β1/Smad3 signaling repressed the inflammatory protein expression in ox-LDL-treated endothelial cells.