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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. 2 — ADM2 reversed the imbalance of M1/M2 polarization induced by AGEs via the PPARγ/IκBα/NF-κB pathway. A Western blot of PPARγ, IκBα, p65, and p-p65 in BMDMs treated with vehicle, AGEs, AGEs+ADM2, and AGEs+ADM2+GW9662. B Quantitative analysis of PPARγ and IκBα protein levels relative to GAPDH and the phosphorylated level of p65. C Representative immunocytochemistry images showing the expression and distribution of p65 in BMDMs in each group. Scale bar 50 μm. D Quantitative analysis of the expression and nuclear translocation of p65. 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