Fig. 5
Vitexin suppressed erastin-induced ferroptosis by regulating NRF2. (A) CCK8 assays were used to assess the viability of HK2 cells exposed to vitexin (100 µM) and pretreated with or without erastin (10 µM). (B) LDH and (C) MDA levels in HK2 cells after treatment with vitexin under basal conditions or after erastin administration. (D) Fluorescence images showing lipid peroxidation stained by the BODIPY-C11 probe (green: oxidized lipids; red: lipids; and blue: Hoechst; scale bar: 10 μm). (E) Western blot analysis of the indicated proteins in NRF2 KO HK2 cells. (F) Cell viability was determined after NRF2 KO or NC HK2 cells treated with erastin and/or vitexin. (G) Fluorescence images of Col1a1 and (H) EdU in NRK-49 F cells that were incubated with HK2-CM (the supernatant of HK2 cells that were pretreated with erastin and/or vitexin, CM: conditioned medium), scale bar = 20 μm. (I) WB was performed to determine E-cadherin protein levels in HK2 cells treated with erastin and/or vitexin. (L) Western blot images showing the protein level of α-SMA in NRK-49 F cells treated with HK2-CM. GAPDH was used as a loading control. The results of three independent experiments are expressed as the mean ± S.D. ****P < 0·0001, ***P < 0·001 (one-way ANOVA for A-C and two-way ANOVA for F)