Fig. 8

IL-13 provides indirect neuroprotection. a, b Neuro2A (a) or SH-SY5Y (b) cells were treated for 72 h with different concentrations of SNAP (µM) with or without IL-13 (ng/ml). IL-13 did not protect against cell death determined by an MTT assay. Data were normalized to untreated control (= dotted black line) and are shown as mean ± SEM. n = 4–5. c, d Representative images of 4-week old neurospheroids obtained from luciferase-expressing hiPSC-NSCs. c Brightfield image of neurosphere. Scale bar = 500 µm. d Immunofluorescent image of neurospheroid showing strong Tuj1 expression. White box region (i) is shown at a higher magnification. Scale bar = 200 µm. e Neurospheroids from luciferase-expressing hiPSC-NSCs were subjected to hypoxic conditions (OGD) for 6 h and were left untreated or were incubated for 48 h with IL-13. No protective effect of IL-13 on cell viability was observed. Data were normalized to untreated control and are shown as mean ± SEM. n = 14–15. f Hippocampal–entorhinal brain slices derived from BALB/c mice were incubated for 72 h with IL-13 (ng/ml) with or without NMDA (100 µM). A low concentration of IL-13 (5 ng/ml) significantly reduced cell death measured via a PI staining. However, even without NMDA administration, a high dose of IL-13 (500 ng/ml) induced cell death. Data were normalized to untreated control and are shown as mean ± SEM. n = 17–38 slices/condition. g Representative images of the PI assay, depicting the hippocampal cornu ammonis (CA) area 1 and 3, showing a decrease in fluorescence intensity when slices were treated with NMDA + IL-13 (5 ng/ml) compared to NMDA treatment alone. DG dentate gyrus. Scale bar = 250 µm. Kruskal–Wallis test with Dunn’s correction (a, b) or one-way ANOVA with Bonferroni post hoc test (e, f). *P < 0.05, **P < 0.01, and ***P < 0.001