ArticleFrontiers in pharmacology2020
Neobavaisoflavone Induces Bilirubin Metabolizing Enzyme UGT1A1 via PPARα and PPARγ.
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 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Metabolic difference of potentially toxic components from Psoraleae Fructus and Euodiae Fructus in Sishen formula by different compatibilities and physiologies.Journal of pharmaceutical analysis · 2026Article
- Emodin Enhances Rosiglitazone's Therapeutic Profile by Dual Modulation of SREBP1-Mediated Adipogenesis and PPARγ-Driven Thermogenesis.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Zinc Supplementation Accelerates Bilirubin Reduction in Neonates with Hyperbilirubinemia: A Double-Blind Randomized Clinical Trial.Reports of biochemistry & molecular biology · 2025Article
- Changes in Serum Bilirubin and Total Bile Acids During Biologic Therapy in Patients with Ulcerative Colitis: A Retrospective Study.Journal of inflammation research · 2025Article
- Flavonoids and Organic Acids Affect Phase II Metabolism based on the Regulation of UGT1A1 Expression and Function.Current computer-aided drug design · 2025Article
- Combination of UGT1A1 polymorphism and baseline plasma bilirubin levels in predicting the risk of antipsychotic-induced dyslipidemia in schizophrenia patients.Schizophrenia (Heidelberg, Germany) · 2024Article
- Induction of cytochrome P450 via upregulation of CAR and PXR: a potential mechanism for altered florfenicol metabolism by macranthoidin BFrontiers in pharmacology · 2024Article
- Bicyclol attenuates high fat diet-induced non-alcoholic fatty liver disease/non-alcoholic steatohepatitis through modulating multiple pathways in mice.Frontiers in pharmacology · 2023Article
- Optical substrates for drug-metabolizing enzymes: Recent advances and future perspectives.Acta pharmaceutica Sinica. B · 2022Review
- The Uridine diphosphate (UDP)-glycosyltransferases (UGTs) superfamily: the role in tumor cell metabolism.Frontiers in oncology · 2022Review
- Calycosin attenuates renal ischemia/reperfusion injury by suppressing NF-κB mediated inflammationFrontiers in pharmacology · 2022Article
- Comprehensive virtual screening of 4.8 k flavonoids reveals novel insights into allosteric inhibition of SARS-CoV-2 MScientific reports · 2021Article
- Lipid-Free PN is Associated with an Increased Risk of Hyperbilirubinemia in Surgical Critically Ill Patients with Admission Hepatic Disorder: A Retrospective Observational Study.Therapeutics and clinical risk management · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
UDP-glucuronosyltransferase 1A1 (UGT1A1) is an essential enzyme in mammals that is responsible for detoxification and metabolic clearance of the endogenous toxin bilirubin and a variety of xenobiotics, including some crucial therapeutic drugs. Discovery of potent and safe UGT1A1 inducers will provide an alternative therapy for ameliorating hyperbilirubinaemia and drug-induced hepatoxicity. This study aims to find efficacious UGT1A1 inducer(s) from natural flavonoids, and to reveal the mechanism involved in up-regulating of this key conjugative enzyme by the flavonoid(s) with strong UGT1A1 induction activity. Among all the tested flavonoids, neobavaisoflavone (NBIF) displayed the most potent UGT1A1 induction activity, while its inductive effects were confirmed by both western blot and glucuronidation activity assays. A panel of nuclear receptor reporter assays demonstrated that NBIF activated PPARα and PPARγ in a dose-dependent manner. Meanwhile, we also found that NBIF could up-regulate the expression of PPARα and PPARγ in hepatic cells, suggesting that the induction of UGT1A1 by NBIF was mainly mediated by PPARs. In silico simulations showed that NBIF could stably bind on pocket II of PPARα and PPARγ. Collectively, our results demonstrated that NBIF is a natural inducer of UGT1A1, while this agent induced UGT1A1 mainly via activating and up-regulating PPARα and PPARγ. These findings suggested that NBIF can be used as a promising lead compound for the development of more efficacious UGT1A1 inducers to treat hyperbilirubinaemia and UGT1A1-associated drug toxicities.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.