ArticleHepatology (Baltimore, Md.)2022
Breviscapine alleviates NASH by inhibiting TGF-β-activated kinase 1-dependent signaling.
Article in Hepatology (Baltimore, Md.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 93 citations in OpenAlex.
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- [Application ofZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
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- The pharmacological effects and therapeutic potential of flavonoids in digestive diseases.Frontiers in pharmacology · 2025Review
- Traditional Mongolian Medicine Qiqirigan-8 alleviates non-alcoholic fatty liver disease via restoring gut microbiota and metabolism.Frontiers in microbiology · 2025Article
- The role of ubiquitination and deubiquitination in the pathogenesis of non-alcoholic fatty liver disease.Frontiers in immunology · 2025Review
- How Traditional Chinese Medicine Can Play a Role In Nanomedicine? A Comprehensive Review of the Literature.International journal of nanomedicine · 2025Review
- TGF-β inhibitors: the future for prevention and treatment of liver fibrosis?Frontiers in immunology · 2025Review
- Metabolism and epigenetics in cancer: toward personalized treatment.Frontiers in endocrinology · 2025Review
- Traditional Chinese medicine for HIV-related chronic comorbidities: evidence and potential therapeutic mechanisms.Frontiers in pharmacology · 2025Review
- Knockdown of hepatic mitochondrial calcium uniporter mitigates MASH and fibrosis in mice.Cell & bioscience · 2024Article
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Authors and funding
18 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsNAFLD is a key component of metabolic syndrome, ranging from nonalcoholic fatty liver to NASH, and is now becoming the leading cause of cirrhosis and HCC worldwide. However, due to the complex and unclear pathophysiological mechanism, there are no specific approved agents for treating NASH. Breviscapine, a natural flavonoid prescription drug isolated from the traditional Chinese herb Erigeron breviscapus, exhibits a wide range of pharmacological properties, including effects on metabolism. However, the anti-NASH efficacy and mechanisms of breviscapine have not yet been characterized. APPROACH AND
resultsWe evaluated the effects of breviscapine on the development of hepatic steatosis, inflammation, and fibrosis in vivo and in vitro under metabolic stress. Breviscapine treatment significantly reduced lipid accumulation, inflammatory cell infiltration, liver injury, and fibrosis in mice fed a high-fat diet, a high-fat/high-cholesterol diet, or a methionine- and choline-deficient diet. In addition, breviscapine attenuated lipid accumulation, inflammation, and lipotoxicity in hepatocytes undergoing metabolic stress. RNA-sequencing and multiomics analyses further indicated that the key mechanism linking the anti-NASH effects of breviscapine was inhibition of TGF-β-activated kinase 1 (TAK1) phosphorylation and the subsequent mitogen-activated protein kinase signaling cascade. Treatment with the TAK1 inhibitor 5Z-7-oxozeaenol abrogated breviscapine-mediated hepatoprotection under metabolic stress. Molecular docking illustrated that breviscapine directly bound to TAK1.
conclusionBreviscapine prevents metabolic stress-induced NASH progression through direct inhibition of TAK1 signaling. Breviscapine might be a therapeutic candidate for the treatment of NASH.
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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.