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. 2021 May 13;12:288. doi: 10.1186/s13287-021-02368-9

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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. 1 — ADM2 reversed AGE-induced M1 macrophage polarization to M2 phenotype. A, B Expression of M1-specific genes (iNOS, IL-6, and TNF-α) (A) and M2-specific genes (Arg-1, MRC1, and TGF-β) (B) of BMDMs treated with vehicle, AGEs, AGEs+ADM2, and AGEs+ADM2+GW9662 was assessed using qRT-PCR. C The expression of CD86 (M1 surface marker) and CD206 (M2 surface marker) on BMDMs in each group was examined using flow cytometry. D Quantification of mean fluorescence intensity (MFI) of the surface markers. E ELISA for production of pro-inflammatory cytokine (TNF-α) and anti-inflammatory, osteogenic cytokines (BMP-2, IGF-1, and TGF-β) in the supernatant of BMDMs in each group. The data were confirmed by one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test from three independently repeated tests and are presented as the means ± SD. *P < 0.05; **P < 0.01