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. 2022 Aug 8;8:353. doi: 10.1038/s41420-022-01146-7

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — 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”.