[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.

[Reduced circulating endothelial progenitor cells is a risk factor of coronary slow flow].

OBJECTIVE: To explore if reduced number of circulating endothelial progenitor cells (EPCs) is a risk factor for patients with coronary slow flow (CSF). METHODS: Thirty patients with CSF and 30 age and gender matched control subjects with normal coronary angiography were included in the study. Mononuclear cells were isolated from peripheral blood by Ficoll density gradient centrifugation and plated on fibronectin-coated culture dishes. EPCs were characterized as adherent cells double positive for DiI-AcLDL-uptake and lectin-binding by converted fluorescence microscope (×200). RESULTS: Smoking, diabetes mellitus, hypertension and the levels of plasma lipoprotein profile were similar between the two groups (all P > 0.05). The number of EPCs was significantly lower in patients with CSF compared with control subjects (35.7 ± 5.9 vs.53.2 ± 5.9, P < 0.01). TIMI frame counts was correlated with circulating EPCs number (OR = 0.424, 95%CI 0.358 - 0.621, P < 0.01) and not associated with gender, age, smoking, diabetes mellitus, hypertension and the levels of plasma lipoprotein profile. CONCLUSION: Decreased circulating EPCs is an independent risk factor for CSF.