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Fig. 5 | Molecular Medicine

Fig. 5

From: Eriodictyol ameliorates cognitive dysfunction in APP/PS1 mice by inhibiting ferroptosis via vitamin D receptor-mediated Nrf2 activation

Fig. 5

Eriodictyol attenuated the cytotoxicity and Tau hyperphosphorylation induced by the Aβ1–42 oligomer in HT-22 cells. A The viability of HT-22 cells was measured using a CCK-8 assay to explore the cytotoxicity of eriodictyol toward HT-22 cells. Cells were treated with eriodictyol (0, 2, 4, 8, 16, 32, 64 or 128 µM) for 48 h. B The viability of HT-22 cells was measured using a CCK-8 assay. HT-22 cells were pre-exposed to eriodictyol (0, 1, 2, 4, 8 or 16 μM) for 2 h and then treated with the Aβ1–42 oligomer (20 μM) for 48 h. C The state and number of HT-22 cells were observed under a microscope. HT-22 cells were pretreated with eriodictyol (0, 2, 4 or 8 μM) and 20 μM Aβ1–42 oligomer for 48 h. D The cytoskeleton of HT-22 cells was stained with FITC-phalloidin. HT-22 cells were treated with eriodictyol (0, 2, 4 or 8 μM) and 20 μM Aβ1–42 oligomer for 48 h after induction with 10 μM RA for 3 days. E Quantification of the neurite length of HT-22 cells using ImageJ software. F Cell death was detected using a propidium iodide assay. G Levels of Tau and p-Tau were measured using Western blotting, and β-actin served as a loading control. The data are presented as the means ± SD of three experiments. *P < 0.05, **P < 0.01 and ***P < 0.001 compared with the Aβ1-42 oligomer group. ###P < 0.001 compared with the control group

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