Aim Although C-reactive protein(CRP) is widely used as an inflammatory marker of cardiovascular disease,statins showed a variety of additional effects that may contribute to their protective vascular benefit.However,it is not fully understood whether CRP exerts direct proinflammatory effects on human vascular endothelial cells(HUVEC). Methods Thrombospondin-1(TSP-1) plays a critical role in the development of atherosclerosis and thrombous.Vascualr endothelial cells were incubated with purified CRP at clinically relevant concentrations(5,10,20 and 40 mg/L).The protein and transcript levels of the TSP-1 were determined by ELISA and RT-PCR respectively.Also,the phosphorylation of p38MAPK was studied via Western blotting analysis. Results In HUVEC,purified CRP significantly induced the protein release and mRNA expression of TSP-1 in a dose-and time-dependent manner respectively.SB₂03580(a specific p38MAPK inhibitor) efficiently suppressed these effects of CRP as well as rosuvastatin(10 μmol/L).CRP triggered the phosphorylation of p38MAPK signal transduction. Conclusion CRP induces TSP-1 protein release and mRNA expression from vascular endothelial cells via activation of the p38MAPK signaling pathways,suggesting that CRP plays an important role in the propagation and prolongation of inflammation in vascular inflammation.