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. 2020 Mar 16;17:21. doi: 10.1186/s12986-020-00440-4

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© The Author(s) 2020

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. 8 — Indirubin enhances BAT activity and induces browning of WAT relying on PKA and p38MAPK signaling pathways. a Western blot analysis performed with the indicated antibodies (Phospho-PKA substrate, UCP1, PGC1α, p-CREB) in differentiated C3H10T1/2 cells on day 6 of brown adipogenesis in present or absent of indirubin and (or) PKA inhibitor. β-tubulin serves as a loading control. b Western blot analysis performed with the indicated antibodies (UCP1, PGC1α) in differentiated C3H10T1/2 cells on day 6 of brown adipogenesis in present or absent of indirubin and (or) p38 MAPK inhibitor. β-tubulin serves as a loading control. c Semi-quantitative analysis of p-p38/p38 ratio from (B). d Proposed model for the role of indirubin in activating BAT and browning of WAT, thus having benefit effects on ameliorating obesity and its associated metabolic dysfunction