©The Author(s) 2026.
World J Diabetes. Feb 15, 2026; 17(2): 112500
Published online Feb 15, 2026. doi: 10.4239/wjd.v17.i2.112500
Published online Feb 15, 2026. doi: 10.4239/wjd.v17.i2.112500
Figure 3 Formononetin intervention delays high glucose-induced senescence in MPC-5 cells.
A: Heatmap of genes related to the p53 signaling pathway showing that formononetin (FN) intervention upregulates MDM2 and CCND1 expression and downregulates p21 expression; B: The molecular docking results of FN and MDM2; C: Western blot bands of proliferating cell nuclear antigen; D and E: Cell staining and cell supernatant β-galactosidase (β-GAL) activity assay demonstrating that FN intervention significantly reduces β-GAL activity in MPC-5 cells; F: Β-GAL indicator cell staining photography (100 ×); G: Western blot analysis revealing that FN intervention significantly decreases proliferating cell nuclear antigen protein levels. n = 3 per group. aP < 0.05 vs control groups; bP < 0.01 vs control groups; cP < 0.05 vs high glucose groups; dP < 0.01 vs high glucose groups. NS: Not significant; FN: Formononetin; HG: High glucose; H-FN: High dose of formononetin; PCNA: Proliferating cell nuclear antigen.
- Citation: Ji Y, Liu RX, He PY, Zhou YM, Li YC, Guo J, Nie B, Liu YN, Liu WJ. Formononetin inhibits p53 signaling pathway activation to delay cellular senescence and ameliorates diabetic kidney disease. World J Diabetes 2026; 17(2): 112500
- URL: https://www.wjgnet.com/1948-9358/full/v17/i2/112500.htm
- DOI: https://dx.doi.org/10.4239/wjd.v17.i2.112500