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. 2023 Jul 26;65:102826. doi: 10.1016/j.redox.2023.102826

Fig. 5.

Fig. 5

WBP2 decelerated ferroptosis in CP-AKI in vivo. A DHE staining revealed that WBP2 overexpression alleviated, while WBP2 knockdown aggravated, cisplatin-induced oxidative stress in kidneys; B & D WBP2 overexpression attenuated, while its gene disruption accentuated, cisplatin-induced increase in 4-HNE levels in the renal cortex, as validated by the immunofluorescence staining (n = 4; *P < 0.0001 compared with Ad-NC or Ad-shNC group, #P < 0.0001 compared with Ad-NC + CP or Ad-shNC + CP group, 1-way ANOVA with Dunn's multiple comparisons); C & E Cisplatin-induced decreased in GPX4 activity was modulated by the expression profile of WBP2 in kidneys (n = 4; *P < 0.0001 compared with Ad-NC or Ad-shNC group, #P < 0.0001 compared with Ad-NC + CP or Ad-shNC + CP group, 1-way ANOVA with Dunn's multiple comparisons); F-G Cisplatin-induced upregulation of FTH1 and downregulation of GPX4 and NCOA4 in kidneys were mitigated by WBP2 overexpression but aggravated by WBP2 knockdown, as detected by western blot studies. CP: cisplatin, Ad-NC: empty vector adenovirus for WBP2 overexpression, Ad-WBP2: adenovirus-mediated WBP2 overexpression, Ad-shNC: empty vector adenovirus for WBP2 knockdown, Ad-shWBP2: adenovirus-mediated WBP2 knockdown. Data are presented as mean ± SD. Scale bars: 100 μm.