ArticleMolecules (Basel, Switzerland)2022
Fraxinellone Induces Hepatotoxicity in Zebrafish through Oxidative Stress and the Transporters Pathway.
Article in Molecules (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Effect of single and repeated-dose oral administration of carbon tetrachloride on liver in zebrafish.Journal of toxicologic pathology · 2026Article
- Preventive and Ameliorative Effects of Alanine Supplementation on High-Fat Diet-Induced Obesity and Metabolic Dysfunction via the Gut-Liver-Adipose Axis in C57BL/6J Mice.Foods (Basel, Switzerland) · 2026Article
- A multi-dimensional computational framework of drug-induced hepatotoxicity: integrating molecular structure features with disease pathogenesis.Briefings in bioinformatics · 2025Article
- Review
- Ganoapplanilactone C fromAntioxidants (Basel, Switzerland) · 2025Article
- Role of PD-1/PD-L1 signaling axis in oncogenesis and its targeting by bioactive natural compounds for cancer immunotherapy.Military Medical Research · 2024Review
- Proteomic analysis of fatty liver induced by starvation of medaka fish larvae.Cell structure and function · 2023Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Fraxinellone (FRA), a major active component from Cortex Dictamni, produces hepatotoxicity via the metabolization of furan rings by CYP450. However, the mechanism underlying the hepatotoxicity of FRA remains unclear. Therefore, zebrafish larvae at 72 h post fertilization were used to evaluate the metabolic hepatotoxicity of FRA and to explore the underlying molecular mechanisms. The results showed that FRA (10-30 μM) induced liver injury and obvious alterations in the metabolomics of zebrafish larvae. FRA induces apoptosis by increasing the level of ROS and activating the JNK/P53 pathway. In addition, FRA can induce cholestasis by down-regulating bile acid transporters P-gp, Bsep, and Ntcp. The addition of the CYP3A inhibitor ketoconazole (1 μM) significantly reduced the hepatotoxicity of FRA (30 μM), which indicated that FRA induced hepatotoxicity through CYP3A metabolism. Targeted metabolomics analysis indicates the changes in amino acid levels can be combined with molecular biology to clarify the mechanism of hepatotoxicity induced by FRA, and amino acid metabolism monitoring may provide a new method for the prevention and treatment of DILI from FRA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.