Fig. 5: Long-term statins administration contributes to lipid accumulation in db/db mice.

All mice were ~50 weeks old. a Clusters of DEGs and KEGG pathway analysis of DEGs in the kidneys of Db and Db + Ato10 groups. n = 3 in each group. b The concentration of TG in kidney. n = 6 in each group. Data are expressed as means ± SEM. c Fluorescence imaging of kidney FFAs uptake from Db/m, Db and Db + Ato10 groups. n = 3 in each group. Data are expressed as means ± SEM. d Representative images of Oil Red O staining. Lipid appear as red spots, as marked by arrows. Original magnification ×200 and ×400. Scale bar: 100 or 50 µm. e Representative images of TEM for LDs. Original magnification ×9700, scale bar: 1 µm. n = 5 images from three mice per group. f Immunohistochemistry of 4-hydroxynonenal (4-HNE) staining. 4-HNE is mainly expressed on the cytoplasmic, and the specific location is indicated by the arrows⁵⁵. Original magnification ×1000. Scale bar: 20 µm. g Immunofluorescence of DHE staining. DHE staining was used to estimate superoxide generation. Arrows represent DHE distribution was markedly increased in the statin administration groups compared to the Db group. Original magnification ×200. Scale bar: 100 µm. n = 10 images from six mice per group (d, f, g). All image part of the kidney was cortex. Renal structures indicated as glomerulus (G), proximal tubule (PT), and distal tubule (DT). One-way ANOVA with Tukey post hoc test was used for the analysis of statistical significance. Source data are provided as a Source Data file.