Copyright: ©Author(s) 2026.
World J Diabetes. Apr 15, 2026; 17(4): 114679
Published online Apr 15, 2026. doi: 10.4239/wjd.v17.i4.114679
Published online Apr 15, 2026. doi: 10.4239/wjd.v17.i4.114679
Figure 5 Hyperoside improves viability and reduces high glucose-induced apoptosis by inhibiting ferroptosis.
bP < 0.01, dP < 0.001. One-way analysis of variance + Tukey’s post hoc test; two-sided. Data are expressed as the mean ± SD; n = 3 independent experiments. A: Cell Counting Kit-8 time course: Control, high glucose (HG) (30 mmol/L), HG + hyperoside (50 μM), and HG + hyperoside (50 μM) + erastin (5 μM); B: Terminal deoxynucleotidyl transferase dUTP nick-end labeling apoptosis; C: Lipid reactive oxygen species; D: Western blot analysis of Nrf2, SLC7A11, and GPX4 expression. HG: High glucose; OD: Optical density; DAPI: 4’,6-diamidino-2-phenylindole; TUNEL: Terminal deoxynucleotidyl transferase dUTP nick-end labeling; DCF: 2,7’-dichlorofluorescein; FITC-A: Fluorescein isothiocyanate-area.
- Citation: Liu C, Li Y, Zhang Y, Gao M, Yang SF. Hyperoside attenuates diabetic nephropathy by activating the Nrf2/SLC7A11/GPX4 axis to restrain ferroptosis. World J Diabetes 2026; 17(4): 114679
- URL: https://www.wjgnet.com/1948-9358/full/v17/i4/114679.htm
- DOI: https://dx.doi.org/10.4239/wjd.v17.i4.114679