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-k B (NF-k B) 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-k B activation in human umbilical vein endothelial cells (HUVECs). By using an electrophoretic mobility shift assays (EMSA), we found that CRP (50mg/ml) increased activation of NF-k B and degradation of inhibitory kappa B (Ik B) in HUVECs, reaching a maximal effect after the incubation with CRP for 1 h. Lovastatin (10.5mol/l) diminished NF-k B activation induced by CRP. Furthermore, lovastatin may block NF-k B activation by causing a stabilization of the Ik B-a in cellular cytoplasm with western blotting analysis. Preincubation of HUVECs with pyrrolidinethiocarbamate (PDTC, NF-k B inhibitor) diminished CD40 expression induced by CRP with flow cytometry. Our results suggest that CRP increases activation of NF-k B and induces CD40 expression in HUVECs partly via activation of NF-k B. Lovastatin, through the inhibition of NF-k B activation, reduces the inflammation involved in the pathogenesis of atherosclerosis.