Fig. 9
aPC reverses hyperglycaemic induced and epigenetically sustained p66Shc expression, promoting atherosclerotic plaque regression in mice. a Experimental design (left top) and representative Oil Red O-stained images of aortic roots (left bottom) and dot plot summarizing data (right). b, c Representative co-immunofluorescence images for p66Shc (b, red), 8-Oxo-dG (c, red), macrophages (MOMA-2, b, c, green), and DAPI nuclear counterstain (b, c, blue; boxed areas shown at higher magnification in the lower panel). Dot plot summarize data for p66Shc-MOMA-2 (b) and 8-Oxo-dG-MOMA-2 co-localization (c, both Icorr, correlation index). Cont: normoglycaemic ApoE−/− mice with normal chow diet; DM: hyperglycaemic ApoE−/− mice; DM-NG-PBS: ApoE−/− DM mice receiving the SGLT2 inhibitor and PBS from week 16 to week 22; DM-NG-aPC: ApoE−/− DM mice with concomitant SGLT2 inhibitor and aPC treatment from week 16 to week 22; DM-NG-aPC-Aza: DM-NG mice with concomitant SGLT2 inhibitor, aPC, and 5-azacytidine. Data shown as dot plots represent mean ± SEM of 8–10 mice per group (a, c); size bars: a–c: 20 µm; **P < 0.01 (one-way ANOVA with Bonferroni-adjusted post hoc comparison of DM and DM-NG-aPC versus control and DM-NG-PBS and DM-NG-aPC-Aza versus DM-NG-aPC)
