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. 2021 Apr 20;16:272. doi: 10.1186/s13018-021-02386-6

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — The effects of CRABP2 overexpression on DEX-induced apoptosis of osteoblast. Osteoblasts were pretreated with a CRABP2 expression plasmid and/or PI3K inhibitor (LY294002) 12 h before DEX treatment. a Flow cytometry after Annexin-V/PI staining analysis of apoptosis after DEX (10^-6 M, 24 h), DEX+ CRABP2 pcDNA3, and DEX+ CRABP2 pcDNA3+LY294002 treatments. b Western blotting was performed to analyze the expression levels of Bax, Bcl-2, cleaved-Caspase-3, Caspase-3, CRABP2 c, PI3K, p-PI3K, AKT, and p-AKT in osteoblast after DEX (10^-6 M, 24 h), DEX+ CRABP2 pcDNA3, and DEX+ CRABP2 pcDNA3+LY294002 treatments. *P<0.05, DEX: dexamethasone