Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease

Figure 7 Formononetin intervention ameliorates podocyte injury and cellular senescence in diabetic kidney disease mice. A: Immunofluorescence staining of podocyte-specific markers (nephrin, podocin, and CD2AP; bars = 50 μm); B: Immunofluorescence staining of fibrosis markers (α-smooth muscle actin; bars = 50 μm); C: Immunofluorescence staining of aging markers (p21; bars = 50 μm); D: Immunofluorescence staining of cellular proliferation dynamics markers (Ki67; bars = 50 μm). n = 4 per group. ^aP < 0.05 vs control groups; ^bP < 0.01 vs high glucose groups. NS: Not significant; IRB: Irbesartan; L-FN: Low dose of formononetin; M-FN: Medium dose of formononetin; H-FN: High dose of formononetin; α-SMA: Α-smooth muscle actin.