Fig. 5
From: Targeting ferroptosis suppresses osteocyte glucolipotoxicity and alleviates diabetic osteoporosis
HGHF enhanced the NRF2–c-JUN interaction. a Effects of HGHF on the levels of MAPK signaling pathway proteins, including p-MKK4, p‐p38/p38, p‐JNK/JNK, p‐ERK/ERK, and c-JUN. b Representative images of bone sections stained with an anti-c-JUN antibody (scale bar: 50 μm). c Effects of HGHF on nuclear import of NRF2. d Effects of HGHF on NRF2 upstream signaling pathway proteins, including LC3, P62 and KEAP1. β-Actin was used as the internal control for cytoplasmic proteins, and Lamin B1 was used as the internal control for nuclear proteins. e Representative images of bone sections stained with an anti-NRF2 antibody (scale bar: 50 μm). f Co-IP results for NRF2 and c-JUN in osteocytes transfected with the NRF2-HA and c-JUN-Myc plasmids. g Co-IP results for endogenous NRF2 and c-JUN in osteocytes. h IF showing that NRF2 colocalized with c-JUN in the nucleus in osteocytes under HGHF treatment (scale bar: 50 μm). i 3D binding structure of NRF2 and c-JUN determined via molecular modeling and docking studies. j Co-IP results for ΔNRF2 and Δc-JUN in osteocytes transfected with plasmids expressing the NRF2-HA and c-JUN-Myc truncations. All data are from n = 3 independent experiments
