Figure 5.
Nrf2 silencing enhances the ferroptosis induced by hemin in EPs from patients with SCD. (A) Immunoblotting showing the effect of shNRF2 and hemin treatment on the expression of NRF2 and ferroptosis stress response proteins in 12-day cultured EPs from patients with SCD. (B-C) Cell proliferation (B) and viability (C) of EPs from patients with SCD cultured with TFMB-L2HG, hemin, or both at the indicated concentrations. (D-E) Effect of TFMB-L2HG (250 μM) and hemin (20 μM) treatment on ferroptosis stress response proteins in EPs from patients with SCD via immunoblotting (D), and flow cytometry analysis of lipid peroxidation levels stained with C11-Bodipy (E). Data represent the mean ± SD of 3 biological replicates. In panel A, a one-way ANOVA with Bonferroni multiple comparison test was used for statistical analysis. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. Ctrl, control.

Nrf2 silencing enhances the ferroptosis induced by hemin in EPs from patients with SCD. (A) Immunoblotting showing the effect of shNRF2 and hemin treatment on the expression of NRF2 and ferroptosis stress response proteins in 12-day cultured EPs from patients with SCD. (B-C) Cell proliferation (B) and viability (C) of EPs from patients with SCD cultured with TFMB-L2HG, hemin, or both at the indicated concentrations. (D-E) Effect of TFMB-L2HG (250 μM) and hemin (20 μM) treatment on ferroptosis stress response proteins in EPs from patients with SCD via immunoblotting (D), and flow cytometry analysis of lipid peroxidation levels stained with C11-Bodipy (E). Data represent the mean ± SD of 3 biological replicates. In panel A, a one-way ANOVA with Bonferroni multiple comparison test was used for statistical analysis. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. Ctrl, control.

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