Fig. 4

CAPE reduced mitochondrial damage by regulation of the SIRT1/PGC1α/DRP1 axis. A Binding of SIRT1 and CAPE within the 3D structure of the complex, the electrostatic surface of proteins and the detail binding mode of ligand with protein. B WB analysis of SIRT1 levels in HMGB1-stimulated BV-2 microglial cells after CAPE treatment for 3 h; n = 3. β-actin was used as the control. C Bar graph showing a quantitative analysis of SIRT1 expression; n = 3. D Representative immunofluorescence images of SIRT1 (red) and IBA-1 (green) within HMGB1-stimulated BV-2 microglial cells after CAPE treatment for 3 h; n = 3. E WB analysis of DRP1 and PGC1α levels within HMGB1-stimulated BV-2 microglial cells after CAPE treatment for 3 h; n = 3. β-actin was used as the control. F, Bar graph showing a quantitative analysis of PGC1α expression; n = 3. G Bar graph showing a quantitative analysis of DRP1 expression; n = 3. H Representative immunofluorescence images of DRP1 (red) and IBA-1 (green) within HMGB1-stimulated BV-2 microglial cells after CAPE treatment for 3 h; n = 3. I Representative immunofluorescence images of TOM20 (red) and IBA-1 (green) within HMGB1-stimulated BV-2 microglial cells after CAPE treatment; n = 3. Scale bar = 50 μm. J Representative immunofluorescence images of ROS (green) within HMGB1-stimulated BV-2 microglial cells after CAPE treatment; Scale bar = 50 μm. K Microglial mitochondrial membrane potential analyzed by JC-1 staining; Scale bar = 50 μm. Data are shown as means ± SEM. Statistical significance was determined with one-way ANOVA followed by Tukey’s post hoc test. ^#p < 0.05 vs. Control group, *p < 0.05 vs. HMGB1 group, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, n.s. = no significance