Figure 6.

Adipose-derived exosomal miRNA-122-5p mediates obesity's protective effects on the pulmonary endothelial barrier and pathological fibroproliferation by inhibiting EndMT and oxidative stress in mice with ARDS. (a) The red fluorescence PKH-26 dye in the CD31-marked pulmonary capillaries confirmed the efficient uptake of exosome in mouse model of ARDS. Scale bar = 50 μm. Histopathologic alterations by H&E (b) and Masson's trichrome staining (c), and ROS production (d) in the lung tissue of mice with ARDS, which were pretreated with adipose-derived exosomes (100 μg/mL in a total volume of 300 μL of PBS every week for three weeks) transfected with miR-122-5p agomir (10 nmol) or miR-122-5p antagomir (50 nmol), as well as their respective negative control (NC). Representative images are shown from three replicated independent experiments. n = 3 mice per group. The PaO₂ (e), BALF protein (f), EBDA extravasation (g), wet/dry ratio (h), collagen content (i), and free GSH concentration (j) in mice with ARDS that were pretreated with adipose-derived exosomes, which were transfected with miR-122-5p agomir or miR-122-5p antagomir or respective NC. n = 5 mice per group in three replicated independent experiments. (k) Western blot analysis of the protein expression of TGFβR1 in the lung tissue. (l) Western blot analysis of the protein expression of VE-cadherin, β-catenin, α-SMA, and Vimentin in the lung tissue. Relative abundances of protein bands were normalized to β-actin as shown in the bar graphs. n = 3 mice per group analyzed in three replicated independent experiments. Data are presented as mean ± S.D. Significant differences are shown by ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001.