Fig. 6

HGHF-induced HO-1 expression was dependent on the NRF2–c-JUN interaction. HGHF-induced HO-1 expression was dependent on the NRF2–c-JUN interaction. a WB results for osteocytes transfected with the indicated siRNA or scrambled siRNA. b Semiquantitative analysis of WB results. c Hmox1 mRNA expression under the indicated treatments was determined using RT–qPCR. d Hmox1 promoter activity under treatment with various concentrations of HGHF was assessed using a dual-luciferase reporter assay. e Hmox1 promoter activity under the indicated treatments was assessed using a dual-luciferase reporter assay. f Schematic representation of the mouse Hmox1 promoter region, including the AREs. g Osteocytes were transfected with the −4 100/+50 promoter construct (WT) or a mutant −3 900/+50 construct (with deletion of the AREs, ΔAREs), and Hmox1 promoter activity was assessed using a dual-luciferase reporter assay. h Osteocytes were treated as indicated for 24 h, and ChIP assays were performed with an anti-NRF2 antibody or normal IgG to detect AREs. i Schematic illustration of the proposed molecular mechanism underlying osteocyte ferroptosis in DOP. HGHF-induced HO-1 expression was dependent on the NRF2–c-JUN interaction. *P < 0.05; **P < 0.01. “NS” indicates nonsignificant. All data are from n = 3 independent experiments