Apoprotein A1Contributes To Modu-lating Polarity Change In Mice Marrow-derived Macrophage

Aim：To explore the anti-inflammatory mechanisms of high densitylipoprotein (HDL) by observing the effects of apolipoprotein A-I (ApoA1),a major protein component of HDL, on the mouse bone barrowmacrophage polarity conversion and the expression of Toll like receptor4(TLR4),myeloid differentiation factor88(MyD88), interferon regulatoryfactor5(IRF5)mRNA.Methods：We used macrophages derived from C57/BL mice bonemarrow were induced by macrophage-colony stimulating factor(M-CSF）for7days, as the source of macrophage in vitro.Macrophages wererandomly divided into six groups,the control group (without giving anydrug intervention), model group (LPS+γ-IFN cultured for24hours),treatment group (respectively5,10,15mg/L apoA1incubated for24hours), the intervention group (first given10mg/L apoA1preincubatedfor24hours, the medium was changed after giving LPS+γ-IFN incubated for24hours).The expression of membrane molecules CD16/32,CD206were detected using fluorescence activated cell sorting (FACS);Enzyme-linked immunosorbent assay (ELISA) were used to detect thesecretion of interleukin-10(IL-10) and IL-12; Real-time quantitativepolymerase chain reaction were used to detect the expression of TLR4,MyD88, IRF5mRNA.Results：After incubation mice marrow-derived macrophage withApoA1(5,10,15mg/L) for24h, the expression of CD16/32, IL-12wasdecreased, expression of CD206, IL-10expression was elevated, and theexpression of TLR4, MyD88, IRF5mRNA was decreased. Afterpre-incubation with apoA1, the expression of CD16/32, IL-12wasdecreased, expression of CD206and IL-10was elevated, and theexpression of TLR4, MyD88, IRF5mRNA was decreased inmacrophages.Conclusion： ApoA1enhances the switch of macrophages toanti-inflammatory macrophages, which may be related with the inhibitionof TLR4-MyD88-IRF5pathway.