Hyperoside attenuates diabetic nephropathy by activating the Nrf2/SLC7A11/GPX4 axis to restrain ferroptosis

Figure 2 Hyperoside ameliorates high glucose-induced oxidative injury in HK-2 cells. ^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: Lactate dehydrogenase, malondialdehyde, Fe²⁺, and glutathione in normal glucose, high glucose (HG), HG + hyperoside (50 μM), and HG + ferrostatin-1 (1 μM); B: Lipid reactive oxygen species using flow cytometry; C: MRNA expression of Nrf2, SLC7A11, and GPX4 detected using quantitative reverse transcription-polymerase chain reaction; D: Protein levels measured using Western blot. NG: Normal glucose; HG: High glucose; Fer-1: Ferrostatin-1; LDH: Lactate dehydrogenase; MAD: Malondialdehyde; FITC-A: Fluorescein isothiocyanate-area; DCF: 2’,7’-dichlorofluorescein.