Objective:The accumulating evidence suggests that C-reactive protein (CRP) may have direct inflammatory effects on the vascular wall and that statin therapy may have important non-lipid anti-inflammatory effects confirmed by decreasing serum inflammatory markers, such as CRP. However, the effect of pravastatin on interleukin-6 (IL-6) gene expression and release in cultured human monocytes from patients with acute coronary syndrome(ACS) was not investigated. Method: A prospective, human monocyte culture, statins intervention study. Monocytes were isolated from blood of patients with ACS and healthy volunteers by the Ficoll density gradient and stimulated by CRP (20 μg/ml)for 24 h. Also 0.1×10 -6, 1×10 -6,5×10 -6, 1×10 -5 mol/L pravastatin coincubated with cells in the presence of CRP. Measurements of supernatants of culture medium IL-6 were performed in duplicate using a commercial assay kit. The expression of IL-6mRNA was determined by RT-PCR method. Result: CRP induced the release of IL-6, with significantly elevated levels in cultured supernatants in ACS group, SA group and healthy group compared with their control respectively. A greater increase of IL-6 induced by CRP was detected in ACS group than in the other groups. CRP induces IL-6mRNA expression in monocytes from patients with ACS. Pravastatin significantly inhibited the expression and production of IL-6 in monocytes stimulated by CRP in a dose-dependent manner. Conclusion:CRP could induce more IL-6 release in human monocyte from patients with ACS than from healthy volunteer and stable angina patients,which may contribute to the mechanism of coronary artery disease in addition to being an incidental product of various types of systemic inflammation. Pravastatin could inhibit this response in a dose-dependent manner in ACS group, which may provide a new insight into the mechanisms of anti-inflammatory or anti-atherosclerotic actions of pravastatin.