Fig. 8
VDR is the key mediator of the regulation of the Nrf2/HO-1 signaling pathway by eriodictyol. A VDR was successfully knocked out by using CRISPR/CAS9 technology. B The viability of HT-22 cells was tested using the CCK-8 assay. Aβ1–42 oligomer (20 μM)-induced normal or VDR knockout HT-22 cells were treated with or without eriodictyol (8 μM) for 48 h. C The levels of Tau, p-Tau, GPX4, VDR, Nrf2, p-Nrf2 and HO-1 in HT-22 cells and sgVDR HT-22 cells were measured using Western blots. D The levels of Nrf2 in the nucleus and cytoplasm of HT-22 cells and sgVDR HT-22 cells were measured using Western blot. E The interaction between VDR and Nrf2 was explored by performed a coimmunoprecipitation assay. F The VDR and GPX4 expression levels in the cortex and hippocampus of normal elderly individuals (G1) and patients with AD (G2) were explored by performing an analysis of differentially expressed genes. G The relationship between Nrf2 and VDR expression in humans, R = 0.22, P = 0.208. The data are presented as the means ± SD of three experiments. *P < 0.05 compared with the control group. ###P < 0.001 compared with Aβ1–42 oligomer group. @P < 0.05 compared with the VDR knockout group