Fig. 5

Edaravone protects miMNs from H₂O₂-induced neurotoxicity. (A and B) iPSC1-derived miMNs (day 7 of differentiation) were pre-treated with edaravone (10 μM) for 16 h in neurotrophic factor-free medium followed by H₂O₂ treatment (25 μM, 24 h). After Calcium AM staining (A, Bar = 10 μm), neurite length was quantified (B, 6 wells for each condition as technical replicates). Edaravone rescues H₂O₂-induced neurite damage. (C and D) iPSC1-derived miMNs (day 25 of differentiation) were pre-treated with edaravone (10 μM) in neurotrophic factor-free medium for 16 h followed by H₂O₂ treatment (3 μM, 24 h). Representative traces (C) show spontaneous spiking activity that was quantified (D, top panel) and compared using values normalized to 0 h (D, bottom panel). Each condition has 3 wells as technical replicates. Edaravone restores spontaneous spiking activity impaired by H₂O₂. (E and F) iPSC1-derived miMNs (day 7 of differentiation) were pre-treated with edaravone (10 μM) for 16 h in neurotrophic factor-free medium followed by glutamate treatment (200 μM, 24 h). After Calcium AM staining (E, Bar = 10 μm), neurite length was quantified (F, 6 wells for each condition as technical replicates). Edaravone rescues glutamate-induced neurite damage. Data represents Mean ± SEM with p values (one-way ANOVA with Tukey’s HSD pos-hoc test) shown inside each panel