The role of C-reactive protein (CRP) in atherogenesis has been supported by more recent data. Some studies have demonstrated marked up-regulation inflammatory responses in endothelial cells subjected to CRP. The nuclear factor-κB (NF-κB) signal transduction is known to play a key role in the expression of these proatherogenic entities. Statins have anti-inflammatory properties independent of their cholesterol-lowering effects. Therefore, we studied the effects of CRP and lovastatin on NF-κB activation in human umbilical vein endothelial cells (HUVECs). By using an electrophoretic mobility shift assays (EMSA), we found that CRP (50 μg/ml) increased activation of NF-κB and degradation of inhibitory kappa B (IκB) in HUVECs, reaching a maximal effect after the incubation with CRP for 1 h. Lovastatin (10⁻⁵ mol/l) diminished NF-κB activation induced by CRP. Furthermore, lovastatin may block NF-κB activation by causing a stabilization of the IκB-α in cellular cytoplasm with western blotting analysis. Preincubation of HUVECs with pyrrolidinethiocarbamate (PDTC, NF-κB inhibitor) diminished CD40 expression induced by CRP with flow cytometry. Our results suggest that CRP increases activation of NF-κB and induces CD40 expression in HUVECs partly via activation of NF-κB. Lovastatin, through the inhibition of NF-κB activation, reduces the inflammation involved in the pathogenesis of atherosclerosis.