Biol. Pharm. Bull. 28(9) 1630—1634 (2005)

active protein (CRP) is a prototypic marker of inflammation, and has been shown in numerous prospective studies to predict cardiovascular events. CRP is both a risk marker and evolved to promote atherogenesis. To date, it has been shown that in endothelial cells, CRP increases the expression of cell adhesion molecules, monocyte-chemotactic protein-1, endothelin-1 and plasminogen activator inhibitor-1, and decreases expression and activity of eNOS and release of prostacyclin. However, CD40-CD40L system is also proven to be an important mediator of several auto-immune and chronic inflammation diseases. Moreover, the investigations identify CD40-CD40L as a key regulator of this process and recognize it as potentially important atherosclerotic therapeutic target. Nuclear factor NF-kB (NF-kB) has been implicated as a key mediator of atherosclerosis. Most proinflammatory genes expressed in endothelial cells during the initial phase of lesion formation and in response to inflammatory mediators are dependent on NF-kB activation. For example, CRP induces IL-8 synthesis and secretion in human aortic endothelial cells via up-regulation of NF-kB activity. Statins are effective lipid-lowering agents, extensively used in medical practice. In vitro and in vivo findings have indicated that statins, beside their lipid-lowering effects, possess anti-inflammatory properties. Some reports have show that lovastatin and atorvastatin reduce pro-inflammatory cytokine expression in smooth muscle cells and mononuclear cells through the inhibition of NF-kB activity. Our previous study demonstrated that CRP resulted in a timeand dose-dependent increase in the cell-surface expression of CD40 and CD40L and lovastatin reduced the expression of CD40 and CD40L induced by CRP in human umbilical vein endothelial cells (HUVECs). However, the mechanisms underlying this association are not completely understood. So, we sought to investigate the effect of CRP on NF-kB activation and inhibitory kappa B (IkB), and whether lovastatin could modulate NF-kB activity induced by CRP in HUVECs.