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. 2023 Jun 8;14:3368. doi: 10.1038/s41467-023-39118-9

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© The Author(s) 2023

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 10 — a Pictures showing H&E or Mason staining of liver sections in BDL mice with or without PCN and nomilin supplementation. Nomilin effectively attenuated the BDL-induced liver damage in WT (upper), but not in PXR^-/- mice (bottom). b Bar-graphs showing the levels of serum ALT and AST in sham or BDL mice (n = 7 for BDL + NML and BDL + PCN, n = 8 for BDL). The data are shown as mean ± SEM. p-values were determined by one-way ANOVA test. ***p < 0.001 vs BDL group. c, d The RNA-seq hierarchical clustering heatmap showing differentially expressed genes (c) and genes in the detoxification process (d) from control (BDL) and nomilin-treated (BDL + NML) mouse liver under BDL surgery. e, f A chart showing the downregulated (e) and up-regulated (f) differentially expressed genes of KEGG pathways compared with the control group in both nomilin-treated and long lifespan mice. g A chart showing the top 20 up-regulated (blue) and downregulated (pink) molecular functions and biological processes (GO). h A diagram depicting the effects of nomilin on longevity through the activation of nuclear hormone receptors and detoxification signalling in C. elegans and mice.