[Anti-inflammation of simvastatin by polarization of murine macrophages from M1 phenotype to M2 phenotype].

OBJECTIVE: To explore the effects of statin on pro-inflammatory macrophage phenotype in a murine M1 macrophage model. METHODS: Macrophages isolated from murine bone barrow were stimulated with interferon-gamma (IFN-γ) and lipopolysaccharide (LPS) to establish a M1 macrophage model. And 1.0, 2.5, 5.0 µmol/L of simvastatin were added to M1 macrophages for a 9-hour culture. Cell surface markers CD16/23 and CD206 were detected by fluorescence activated cell sorter (FACS) and interleukin-10 (IL-10) and IL-12 by ELISA. RESULTS: The CD16/32 expression was 86.39% ± 2.24% and IL-12 secretion (1562 ± 217) pg/ml in IFN-γ and LPS-stimulated macrophages. After a 9-hour incubation with 1.0, 2.5, 5.0 µmol/L simvastatin, the CD206 expression levels were 68.10% ± 2.48%, 75.28% ± 1.66%, 86.32% ± 2.19% and the secretion of IL-10 (500 ± 5), (675 ± 28) and (916 ± 15) pg/ml respectively. By analysis of variance and q test of mean, the difference was statistically significant (all P < 0.01) between the groups of M1 model (9.67% ± 5.48%, (298 ± 11) pg/ml) . And the phenotypic features were similar to those of the groups of M2 model. CONCLUSION: Simvastatin may inhibit inflammation by enhancing the switching of M1 macrophage to M2 macrophage phenotype.