Fig. 7.

aPC reverses the glucose-induced and sustained pro-atherogenic phenotype of macrophages. a, b Representative co-immunofluorescence images (a, left panel) for 8-Oxo-dG (green; DAPI nuclear counterstain, blue) and immunoblots images (out of three independent repeat experiments with two technical replicates each) for nitrotyrosine (Nitro, b, top; GAPDH: loading control) of BMDMs with treatment as indicated and dot plot summarizing data (a, right panel, b, bottom). c Representative reverse-transcriptase-PCR gel images (out of three independent repeat experiments with two technical replicates each) for IL-6 and TNF-α (right panel; β-actin: loading control) and dot plot summarizing data (middle and right panels, respectively). d Representative immunoblot images (out of four independent repeat experiments with two technical replicates each) for NF-κB p65 (top panel; GAPDH: loading control) and dot plot summarizing data (bottom). e Representative Oil Red O images reflecting lipid uptake into BMDMs (left panel) and dot plot summarizing data (right panel). NG: normal glucose (5 mM glucose plus 20 mM mannitol, 48 h), HG: high glucose (25 mM, 48 h), HG-NG: HG (48 h) followed by NG (24 h) condition; HG-NG-aPC: HG-NG conditions with additional exposure to aPC (20 nM) during the last 24 h). Data shown as dot plots represent mean ± SEM of at least three independent repeat experiments with at least two technical replicates each; **P < 0.01 (one-way ANOVA with Bonferroni-adjusted post hoc comparison of HG and HG-NG versus NG and HG-NG-aPC versus HG-NG). Uncropped immunoblots for Fig. 7b, d and reverse-transcriptase-PCR gel images for Fig. 7c are provided in Supplementary Figure 22