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 3 Hyperoside confers protection against erastin-induced ferroptotic injury.
aP < 0.05, bP < 0.01, cP < 0.001, 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 times course (0-48 hours): Control, erastin (5 μM), and hyperoside (50 μM) + erastin; B: Lactate dehydrogenase, malondialdehyde, Fe2+, and glutathione; C: Lipid reactive oxygen species; D: Terminal deoxynucleotidyl transferase dUTP nick-end labeling apoptosis; E: Western blot of Nrf2, SLC7A11, and GPX4. LDH: Lactate dehydrogenase; MAD: Malondialdehyde; OD: Optical density; GSH: Glutathione; FITC-A: Fluorescein isothiocyanate-area; DAPI: 4’,6-diamidino-2-phenylindole; TUNEL: Terminal deoxynucleotidyl transferase dUTP nick-end labeling.
- 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