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. 2022 Feb 8;28:19. doi: 10.1186/s10020-022-00444-1

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© The Author(s) 2022

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/.

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Fig. 5 — UA treatment inhibited myocardial fibrosis via Nrf2 pathway in vivo. A Represent images by H&E staining of heart tissues from indicated groups and statistic score of injury level. B Represent images by Masson’s trichrome staining of heart tissues from indicated groups and statistic results of the fibrosis area. C The mRNA levels and D protein levels of fibrosis markers including vimentin, DDR2, tensin and α-SMA in heart tissues from indicated groups. E The protein levels of Nrf2, SOD1, HO-1 and NQO1 in heart tissues from indicated groups. β-actin was used as normalized control. *P < 0.05, **P < 0.01, ***P < 0.001