Fig. 4: Cpd16-induced Nrf2 activation and osteoblasts protection against H2O2 were stronger than other known Nrf2 activators.

The primary murine osteoblasts (A, B), human osteoblasts (F), and MC3T3-E1 murine osteoblastic cells (G) were treated with 25 μM of Cpd16, Sulforaphane (SFH), 4-octyl itaconate (4-OI), tert-butylhydroquinone (TBHQ), and cultured for 6 h, the relative ARE activity (A) and HO1 mRNA (B, F, G) expression were tested. The primary murine osteoblasts were pretreated with 25 μM of Cpd16, SFH, 4-OI, or TBHQ for 2 h, followed by H2O2 (400 μM) stimulation, and viability, apoptosis, and necrosis were measured through CCK-8 (C), TUNEL-nuclei staining (D), and LDH releasing (E) assays, respectively. *P < 0.05 versus “Veh”. #P < 0.05. versus “Cpd16”.