Figure 3.

Transferrin protects RGCs against different cell-death mechanisms. Activation of apoptosis, necrosis, or ferroptosis in rat retinal explants exposed to FeSO₄ (A), NMDA (B) or CoCl₂ (C) in presence or in absence of TF was monitored by, respectively, the quantification of TUNEL-positive RGCs and by the change in RIP3 or GPX4 immunostaining intensity in RGC layer compared to controls (fold change). (A) FeSO₄ induces a significant increase in RIP3 and GPX4 expression which was limited or prevented by co-treatment with TF. (B) NMDA increases the number of TUNEL-positive cells as well as RIP3 and GPX4 expression. TF prevents increase in all three markers. (C) CoCl₂ induces a significant increase in the number of TUNEL-positive cells which was prevented by TF. Data represent means ± SEM, n = 4–10 explants per condition. Statistical analysis was performed with Kruskal–Wallis and Dunn’s tests for multiple comparisons. ns, not significant; # p < 0.05; ## p < 0.01; ### p < 0.001; #### p < 0.0001 compared to control. ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001 compared to stress condition.