Fig. 7
Effect of PM2.5, the DRP1 inhibitor Mdivi-1 and the OPA1 activator BGP-15 on airway hyper-responsiveness (AHR) in mice. Mean percentage increase in lung resistance (RL) to increasing concentrations of acetylcholine (A). *P < 0.05, **P < 0.01, and ***P < 0.001 compared with control mice, &P < 0.05, &&P < 0.01, and &&&P < 0.001 compared with the DRP1 inhibitor (Mdivi-1) + PM2.5 mice, %P < 0.05, %%P < 0.01, and %%%P < 0.001 compared with the OPA-1 activator (BGP-15) + PM2.5 mice. Individual and mean –logPC100, an indicator of bronchial responsiveness. n = 8 in each group (B). Individual and mean airway resistance (C-E) or compliance (F-H) at 0 (C, F), 128 (D, G) and 256 mg/L (E, H) of acetylcholine. Representative photomicrographs of mouse lung tissues in hematoxylin and eosin (H&E)-stained sections from control distilled water instilled mice, PM2.5-instilled mice, Mdivi-1-pretreated PM2.5-instilled mice and BGP-15-pretreated PM2.5-instilled mice (I, original magnification, x10). Individual and mean values of inflammation scores measured from H&E-stained sections (J). Representative pictures of SFTPC immunofluorescence staining in the lung tissues of PM2.5, Mdivi-1- and BGP-15-treated cells are shown (K, original magnification, x10). Graphical analysis of SFTPC/DAPI fluorescence area (L) and SFTPC fluorescence (M). One-way ANOVA with Bonferroni’s post hoc test (for equal variance) or Dunnett’s T3 post hoc test (for unequal variance) was performed for comparisons among multiple groups. *P < 0.05, **P < 0.01, ***P < 0.001