Figure 4

RAGE-apt ameliorates the progression of MR-associated podocyte injury through the inhibition of oxidative stress production and Rac1 activation. (a and b) SBP levels in Cont, DOCA-Ctrl-apt, DOCA–RAGE-apt, and DOCA-Spiro mice (n = 4–12 per group), ^†p < 0.05 vs Cont, ^$p < 0.05 vs DOCA-Spiro, (c) UAE levels (n = 4–12 per group), (d) podocin expression (n = 4–5 per group), (e) double staining for nitrotyrosine and CML by immunofluorescence (n = 4–5 per group), (f) glomerular CML staining by immunohistochemistry (n = 4–5 per group), (g) plasma CML levels (n = 4–12 per group), (h) glomerular RAGE expression (n = 4–5 per group), (i) cortical RAGE protein expression by Western blot (n = 4 per group), (j and k) glomerular GTP-bound Rac1 and MR expression (n = 4–5 per group). Data are presented as mean ± SEM. ^#p < 0.05, ^##p < 0.01 vs DOCA-Ctrl-apt mice, ^†p < 0.05, ^††p < 0.01 vs DOCA-Spiro mice. All kidney sections are 4-μm thin. Bars = 20 μm. RAGE, receptor for advanced glycation end products; MR, mineralocorticoid receptor; SBP, systolic blood pressure; Cont, control; Ctrl-apt, control aptamer; RAGE-apt, RAGE aptamer; UAE, urinary albumin excretion; Spiro, spironolactone; CML, carboxymethyllysine.