BCI inhibits macrophage recruitment in infarcted rat hearts and LPS-induced mouse abdominal macrophages. (A) Experimental scheme showing the timing of BCI injections and MI in rats. (B,C) Percentages of His36+ macrophages in the LV of rats at 7 days post-MI by flow cytometry (B) and statistics of His36+ macrophages (C) (n=3 per group; two hearts per sample). (D) Immunofluorescent staining showing decreased numbers of His36+ macrophages (red) in the LV of rats after BCI treatment at 7 days post-MI compared with vehicle treatment (scale bar: 50 μm). (E) The percentage of His36+ macrophages to DAPI+ cells in each group (n=5 per group). (F) The expression levels of Il1b, Il6, Il12b, Retnla, Arg1 and Ym1 mRNAs were determined in sham and MI hearts (day 7) with or without BCI treatment (n=3–4 per group). (G,H) Percentages of lipopolysaccharide (LPS)-induced CD11b+ (also known as ITGAM+) F4/80+ macrophages in mouse abdominal cells were measured by flow cytometry (G), and statistics of CD11b+ F4/80+ cells are shown (H) (n=3 per group; two mice per sample). (I) LPS-induced IL-1β, IL-6 and IL-12 proteins in mouse serum detected by ELISA (n=5 mice per group). One-way ANOVA followed by Dunnett's multiple comparison test; mean±s.e.m.; *P<0.05, **P<0.01; ns, not significant.
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