Objective: The purpose of this research is to investigate theanti-inflammatory mechanism of statin by changing the polarity ofmacrophages.Methods: Mice bone marrow derived macrophages were stimulated by thelipopolysaccharide (LPS) plus interferon-gamma (IFN-gamma) to establish M1macrophages model and50umol/L of pravastatin sodium was then added for24h. Enzyme-linked immunosorbent assay(ELISA) is used to detect secretion ofinterleukin-10(IL-10) and IL-12; Flow cytometry is used to detect the cellmembrane surface antigen expression of CD16/32, CD206; Real timequantitative polymerase chain reaction (RT-qPCR)is to detect the expression ofTLR4, myeloid differentiation factor88(MyD88) and interferon regulatoryfactor5(IRF5) mRNA.Results: The expression of IL-10, CD206in M1macrophages areincreased while the expression of IL-12, CD16/32and TLR4, MyD88, IRF5mRNA are decreased after treated by pravastatin sodium.Conclusions: Pravastatin sodium may change the macrophage polaritythrough inhibition of the TLR4-MyD88-IRF5signaling transduction pathway,that playing the effect of anti-inflammatory. |