The Change Of Macrophages Polarization By Simvastatin

Objective: Atherothrombotic vascular disease is quickly becoming the leadingcause of mortality worldwide, accounting for a fifth of all deaths.Innateinflammation is a hallmark of both experimental and human atherosclerosis. Thechange of mononuclear macrophages polarity in atherosclerosis(As) happened andthe process of development have the important meaning. Different subtypes ofmacrophage conversion for atherosclerosis treatments with new targets.Statins are3-hydroxy-3-methylglutaryl coenzyme A(HMG-COA) reductase inhibitors, whichare widely used to lower serum cholesterol levels in the primary and secondaryprevention of cardiovascular disease. Evidence suggests that statins haveantiinflammatory property in addition to their lipid lowering effect. Macrophagesare heterogeneous and include classically activated M1and alternatively activatedM2macrophages, characterized by pro-and anti-inflammatory functions,respectively. In the present study, we investigated the influence of statin onpro-inflammatory macrophage phenotype in a mouse M1macrophage model.Methods: Macrophage isolated from mouse barrow were stimulated withIFN-γ and lipopolysaccharide to establish a M1macrophage model. M1macrophage model were divided into5group: normal contorl, simvastatin3 groups:1，2.5，5μmol/L of simvastatin were added to M1macrophage for culturefor9h, absolute ethyl alcohol group. CD16/32， CD206were detected byFACS;IL-10and IL-12were detected by ELISA.Results: Two markers of the M2phenotype, CD206and IL-10underwentsignificant increases after treatment with simvastatin while markers of the M1phenotype did not undergo any significant change. Hence, cells that hadundergone this treatment were confirmed as exhibiting the M2macrophagephenotype.Conclusion: Simvastatin may inhibit inflammation by enhancing the switching ofM1macrophage to M2macrophage phenotype.