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Fig. 5 | Molecular Medicine

Fig. 5

From: Downregulation of HMGB1 carried by macrophage-derived extracellular vesicles delays atherosclerotic plaque formation through Caspase-11-dependent macrophage pyroptosis

Fig. 5

Macrophage-EV/siHMGB1 suppresses the release of HMGB1 expression to inhibit foam cell formation and inflammatory responses in macrophages. A Expression of HMGB1 in macrophages treated with ox-LDL and intervened with MEV/siHMGB1 was detected by Western blotting. B HMGB1 content in the macrophage culture supernatants after macrophage-EV/siHMGB1 or ox-LDL treatment measured by ELISA. C Lipid droplet in macrophages to reflect foam cell formation analyzed by Oil red O staining. D Uptake of Dli-labeled ox-LDL by macrophages determined by IF (400 × , 25 μm). E Foam cell formation in plaque tissues of AS mice after macrophage-EV/siHMGB1 treatment assessed by Oil red O and F4/80 staining (400 × , 25 μm). F Levels of TNF-α and IL-6 in the macrophage culture supernatants studied by ELISA. G Macrophage polarization measured by flow cytometry. H Macrophage polarization in the plaque tissues of AS mice tracked by IF. I Expression of LOX-1, SR-A, and CD36 in macrophages treated with ox-LDL and intervened with MEV/siHMGB1 by Western blot analysis. iNOS is the M1-type macrophage marker, while CD206 is an M2-type macrophage marker. *Indicates p < 0.05. Data among multiple groups are compared using one-way ANOVA, followed by Tuckey’s post hoc test

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Molecular Medicine

ISSN: 1528-3658