ArticleJournal of translational medicine2024
Bifidobacterium adolescentis-derived hypaphorine alleviates acetaminophen hepatotoxicity by promoting hepatic Cry1 expression.
Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed.
- Circadian regulation of hepatic detoxification: implications for drug-induced liver injury.Archives of toxicology · 2026Review
- Urinary Hypaphorine as a Candidate Marker of FFQ-Derived Legume Intake Within the EAT-Lancet Framework in Free-Living Adults.Foods (Basel, Switzerland) · 2026Article
- Article
- Article
- Bifidobacterium bifidum reduces oxidative stress and alters gut flora to mitigate acute liver injury caused by N-acetyl-p-aminophenol.BMC microbiology · 2025Article
- Natural Polyphenol-Mediated Inhibition of Ferroptosis Alleviates Oxidative Damage and Inflammation in Acute Liver Injury.Biomaterials research · 2025Article
- Analysis of gut microbiota-derived metabolites regulating pituitary neuroendocrine tumors through network pharmacology.Frontiers in pharmacology · 2024Article
- Plasma metabolomic signatures of the no-reflow phenomenon in stroke patients following thrombectomy.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
18 authors.
Funding
Abstract
Acetaminophen (APAP)-induced liver injury (AILI) is a pressing public health concern. Although evidence suggests that Bifidobacterium adolescentis (B. adolescentis) can be used to treat liver disease, it is unclear if it can prevent AILI. In this report, we prove that B. adolescentis significantly attenuated AILI in mice, as demonstrated through biochemical analysis, histopathology, and enzyme-linked immunosorbent assays. Based on untargeted metabolomics and in vitro cultures, we found that B. adolescentis generates microbial metabolite hypaphorine. Functionally, hypaphorine inhibits the inflammatory response and hepatic oxidative stress to alleviate AILI in mice. Transcriptomic analysis indicates that Cry1 expression is increased in APAP-treated mice after hypaphorine treatment. Overexpression of Cry1 by its stabilizer KL001 effectively mitigates liver damage arising from oxidative stress in APAP-treated mice. Using the gene expression omnibus (GEO) database, we verified that Cry1 gene expression was also decreased in patients with APAP-induced acute liver failure. In conclusion, this study demonstrates that B. adolescentis inhibits APAP-induced liver injury by generating hypaphorine, which subsequently upregulates Cry1 to decrease inflammation and oxidative stress.
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Registered trials
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