ArticleScientific reports2024
Emodin alleviates cholestatic liver injury by modulating Sirt1/Fxr signaling pathways.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Clinical efficacy and metabolomics profiling of dachaihu decoction for patients with septic liver injury: a randomized controlled trial.Frontiers in pharmacology · 2025Trial
- MicroRNA-SIRT1 crosstalk in liver diseases: molecular regulation of metabolism, inflammation, and cell survival.Molecular biology reports · 2026Review
- The Farnesoid X receptor-bile acid axis contributes to immune evasion in gastric cancer and its inhibition enhances efficacy of anti-PD-L1 therapy.Biochemistry and biophysics reports · 2026Article
- Article
- Attenuation of chlorpyrifos-induced liver injury, oxidative stress and inflammation by selenium nanoparticles via SIRT1/FXR/Nrf2 signaling pathway modulation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- SSRIs-induced liver injury adverse events: a data-based retrospective study and investigation of potential toxicological mechanisms.Frontiers in pharmacology · 2026Article
- To Explore the Active Components, Targets, and Potential Effects of Emodin in the Treatment of Colorectal Cancer Based on Network Pharmacology.PPAR research · 2025Article
- Pharmacological advances in multi-targeted strategies for type 2 diabetes mellitus: a systematic perspective based on traditional Chinese medicine.Frontiers in pharmacology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Emodin (EMO) has the effect of anti-cholestasis induced by alpha-naphthylisothiocyanate (ANIT). But its mechanism is still unclear. The farnesoid X receptor (Fxr) is the master bile acid nuclear receptor. Recent studies have reported that Sirtuin 1 (Sirt1) can regulate the activities of Fxr. The purpose of the current study was to investigate the mechanism of EMO against ANIT-induced liver injury based on Sirt1/Fxr signaling pathway. The ANIT-induced cholestatic rats were used with or without EMO treatment. Serum biochemical indicators, as well as liver histopathological changes were examined. The genes expressions of Sirt1, Fxr, Shp, Bsep and Mrp2 were detected. The expressions of Sirt1, Fxr and their downstream related genes were investigated in vitro. The results showed that EMO significantly alleviated ANIT-induced liver injury in rats, and increased Sirt1, Fxr, Shp, Bsep and Mrp2 gene expression in liver, while decreased the expression of Cyp7a1. EMO significantly activated Fxr, while Sirt1 inhibitor and Sirt1 gene silencing significantly reduced Fxr activity in vitro. Collectively, EMO in the right dose has a protective effect on liver injury induced by ANIT, and the mechanism may be through activation of Fxr by Sirt1, thus regulating bile acid metabolism, and reducing bile acid load in hepatocytes.
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