Aim To investigate the mechanism of statins to prevent and cure atherosclerosis （As） by the study of pravastatin sodium changes mouse macrophages polarity and anti-inflammatory action. Methods Supernatant from L929 cells was used to induce mice bone marrow cells into M0 macrophages,then it was stimulated by LPS plus IFN-γ,and makde into M1 macrophages,after that it was given 50 μmol/L pravastatin sodium,TLR4 specific receptor inhibitor for 12 h,then intervented with inhibition of 50 μmol/L pravastatin sodium.ELISA was used to detect cells secretion factors,such as the level of IL-10 and IL-12.Flow cytometry was to detect the cell membrane surface antigen expression of CD16/32,CD206.Fluorescence quantitative polymerase chain reaction （PCR） was to detect the expression of TLR4,MyD88 and IRF5 mRNA. Results The expression of IL-12,CD16/32 and TLR4,MyD88,IRF5 mRNA in M1 macrophages were increased,but the expression of IL-10,CD206 were higher,TLR4,MyD88,and IRF5 mRNA were lower in macrophages treated by pravastatin sodium （P＜0.05）.Compared with the 50 μmol/L pravastatin sodium group,the effect of TLR4 specific receptor inhibitor for 12 h,then interventing with inhibition of 50 μmol/L pravastatin sodium group was not obvious （P＞0.05）. Conclusions Pravastatin sodium can change macrophage polarity which plays a role of anti-inflammatory.It may affect the TLR4 -MyD88-IRF5 signaling transduction pathway,playing the effect of anti-As.