ArticleFrontiers in pharmacology2025
Ursolic acid drug-drug nanocrystals ameliorate cholestatic liver injury via inhibiting oxidative stress and regulating bile acid metabolism.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Ursolic acid: context-dependent redox activity on oxidative stress and its toxicological implications.Archives of toxicology · 2026Review
- Ursolic acid methyl ester mitigates aluminum oxide nanoparticle-induced hematobiochemical, immune, and oxidative disturbances and modulates apoptosis-related gene expression in Oreochromis niloticus.Veterinary research communications · 2026Article
- Ferroptosis regulatory networks and precision interventions in autoimmune hepatitis: comparison with cholestatic diseases.Frontiers in immunology · 2026Review
- Research Progress and Prospects of Saponins in the Treatment of NAFLD: A Narrative Review.Molecules (Basel, Switzerland) · 2025Review
- Wet Media Milling Preparation and Process Simulation of Nano-Ursolic Acid.Pharmaceutics · 2025Article
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Authors and funding
11 authors.
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Abstract
Introduction: Cholestatic liver injury (CLI) is a liver dysfunction closely associated with oxidative stress and bile acid (BA) metabolic disorders, but effective therapies are lacking.The use of ursolic acid (UA) and Methods: In this study, we synthesized drug-drug nanocrystals (UA-NSps) composed of UA and VES to treat CLI and evaluated their synergistic therapeutic effects by regulating bile acid metabolism and inhibiting oxidative stress in ANIT-induced CLI mice. Results and discussion: Our investigation demonstrated that UA-NSps exhibited high drug-loading capacity, spherical morphology, and improved dissolution and oral bioavailability. In the ANIT model, UA-NSps effectively restored liver function, as evidenced by histopathological and biochemical improvements. Mechanistically, UA-NSps enhanced Nrf2 nuclear translocation, upregulated Nrf2 and HO-1, reduced pro-inflammatory cytokines, and ameliorated mitochondrial damage. Moreover, UA-NSps alleviated the bile acid metabolism disorders by upregulating the transcriptional activity of UGT2B1, BSEP, and MRP2, as well as the protein expression of nuclear receptors and metabolic enzymes PXR,CYP3A4, and UGT1A1. Our study presents a novel drug-drug nanocrystal strategy that enhances the therapeutic efficacy against CLI by inhibiting oxidative stress and regulating bile acid metabolism.
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