Fig. 6

Genetic inhibition of novel-miR-7 ameliorates NAFLD hepatic sEV-induced microvascular endothelial hyperpermeability. MVECs were transfected with 100 nmol/L novel-miR-7 inhibitor or negative control (NC) inhibitor and incubated with or without 120 μg/mL NAFLD hepatic sEVs for 24 h. A Representative western blot bands and the summarized data determined by densitometric analysis, n = 4 per group. B Representative images of acridine orange (AO) and magic red (MR) staining, n = 4 per group. Scale bar, 20 μm. C Representative western blot bands, n = 4 per group. D The summarized data of caspase-1, IL-1β and supernate HMGB1 of WB analysis determined by densitometric analysis, n = 4 per group. E The summarized data of ZO-1 and ZO-2 of WB analysis determined by densitometric analysis, n = 4 per group. F Representative flow cytometry images of caspase-1 FLICA staining, n = 4 per group. G The summarized data of the positive cells of FLICA staning, n = 4 per group. The fold changes were obtained by calculating the ratio of the positive cells of the treated groups to the NC inhibitor group. H Relative permeability of the endothelial monolayer to FITC-dextran, n = 4 per group. Data are expressed as the mean ± SEM. Statistics: One-way ANOVA, **P < 0.01 vs. NC inhibitor group; ^#P < 0.05, ^##P < 0.01 vs. NC inhibitor plus MCD hepatic sEVs group; ^&P < 0.05, ^&&P < 0.01 vs. NC inhibitor group; ^$P < 0.05, ^$$P < 0.01 vs. NC inhibitor plus HFD hepatic sEVs group