ArticleFrontiers in pharmacology2020
LC-MS-Based Metabolomic Study of Oleanolic Acid-Induced Hepatotoxicity in Mice.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Targeting Oxidative Stress in Carcinogenesis: Oleanolic Acid and Its Molecular Pathways.Antioxidants (Basel, Switzerland) · 2026Review
- Antitumour activity of oleanolic acid: A systematic review and meta‑analysis.Oncology letters · 2024Article
- Dose-Response Efficacy and Mechanisms of Orally AdministeredNutrients · 2023Article
- Hepatotoxic mechanism of cantharidin: insights and strategies for therapeutic intervention.Frontiers in pharmacology · 2023Review
- Farnesoid X receptor contributes to oleanolic acid-induced cholestatic liver injury in mice.Journal of applied toxicology : JAT · 2022Article
- Lysophosphatidylcholine: Potential Target for the Treatment of Chronic Pain.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oleanolic acid (OA), a natural triterpenoid, which has the development prospects in anti-tumor therapy is a widely used hepatoprotective drug in China. It has been reported that OA can cause liver toxicity after higher doses or longer-term use. Therefore, the study aims to explore the possible hepatotoxicity mechanism based on liver metabolic profiles. Liver metabolic profiles were obtained from untargeted ultrahigh performance liquid chromatography (UHPLC)-Q Exactive Orbitrap mass spectrometry (MS) technique. It was found that altered bile acid, amino acid, and energy metabolism might be at least partly responsible for OA-induced hepatotoxicity. Bile acid metabolism, as the most important pathway, was verified by using UHPLC-TSQ-MS, indicating that conjugated bile acids were the main contributors to OA-induced liver toxicity. Our findings confirmed that increased bile acids were the key element of OA hepatotoxicity, which may open new insights for OA hepatotoxicity in-depth investigations, as well as provide a reference basis for more hepatotoxic drug mechanism research.
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Registered trials
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