ArticleArchives of toxicology2017
Role of the lipid-regulated NF-κB/IL-6/STAT3 axis in alpha-naphthyl isothiocyanate-induced liver injury.
Article in Archives of toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- Genetic polymorphisms in PXR and NF-κB1 influence susceptibility to anti-tuberculosis drug-induced liver injury.PloS one · 2019Trial
- Functional metabolomics: unlocking the role of small molecular metabolites.Frontiers in molecular biosciences · 2025Review
- Adipokine chemerin overexpression in trophoblasts leads to dyslipidemia in pregnant mice: implications for preeclampsia.Lipids in health and disease · 2023Article
- Integrated Lipidomics and Metabolomics Study of Four Chemically Induced Mouse Models of Acute Intrahepatic Cholestasis.Frontiers in pharmacology · 2022Article
- Novel roles of lipopolysaccharide and TLR4/NF-κB signaling pathway in inflammatory response to liver injury in Budd-Chiari syndrome.World journal of gastrointestinal surgery · 2021Article
- iTRAQ-based quantitative proteomics analysis of the hepatoprotective effect of melatonin on ANIT-induced cholestasis in rats.Experimental and therapeutic medicine · 2021Article
- Metabolomic Analysis Reveals the Therapeutic Effects of MBT1805, a Novel Pan-Peroxisome Proliferator-Activated Receptor Agonist, on α-Naphthylisothiocyanate-Induced Cholestasis in Mice.Frontiers in pharmacology · 2021Article
- Impaired clearance of sunitinib leads to metabolic disorders and hepatotoxicity.British journal of pharmacology · 2019Article
- Lipidomics reveal aryl hydrocarbon receptor (Ahr)-regulated lipid metabolic pathway in alpha-naphthyl isothiocyanate (ANIT)-induced intrahepatic cholestasis.Xenobiotica; the fate of foreign compounds in biological systems · 2019Article
- Celastrol Protects From Cholestatic Liver Injury Through Modulation of SIRT1-FXR Signaling.Molecular & cellular proteomics : MCP · 2019Article
- Protective Effect ofInternational journal of molecular sciences · 2018Article
- Molecular mechanism and research progress on pharmacology of traditional Chinese medicine in liver injury.Pharmaceutical biology · 2018Review
- Targeted Metabolomics Reveals a Protective Role for Basal PPARα in Cholestasis Induced by α-Naphthylisothiocyanate.Journal of proteome research · 2018Article
- Targeting nuclear receptors for the treatment of fatty liver disease.Pharmacology & therapeutics · 2017Review
- Inhibition of JNK signalling mediates PPARα-dependent protection against intrahepatic cholestasis by fenofibrate.British journal of pharmacology · 2017Article
- PPARα activation protects against cholestatic liver injury.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
Abstract
Alpha-naphthyl isothiocyanate (ANIT)-induced liver damage is regarded as a useful model to study drug-induced cholestatic hepatitis. Ultra-performance liquid chromatography coupled with electrospray ionization quadrupole mass spectrometry (UPLC-ESI-QTOF MS)-based metabolomics revealed clues to the mechanism of ANIT-induced liver injury, which facilitates the elucidation of drug-induced liver toxicity. 1-Stearoyl-2-hydroxy-sn-glycero-3-phosphocholine (LPC 18:0) and 1-oleoyl-2-hydroxy-sn-glycero-3-phosphocholine (LPC 18:1) were significantly increased in serum from ANIT-treated mice, and this increase resulted from altered expression of genes encoding the lipid metabolism enzymes Chka and Scd1. ANIT also increased NF-κB/IL-6/STAT3 signaling, and in vitro luciferase reporter gene assays revealed that LPC 18:0 and LPC 18:1 can activate NF-κB in a concentration-dependent manner. Activation of PPARα through feeding mice a Wy-14,643-containing diet (0.1%) reduced ANIT-induced liver injury, as indicated by lowered ALT and AST levels, and liver histology. In conclusion, the present study demonstrated a role for the lipid-regulated NF-κB/IL-6/STAT3 axis in ANIT-induced hepatotoxicity, and that PPARα may be a potential therapeutic target for the prevention of drug-induced cholestatic liver injury.
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