ArticleChinese medicine2025
Baicalin mitigates alcoholic-associated liver disease via SOCS1-driven reprogramming of macrophages.
Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Rapid and Selective Extraction and Detection of Baicalin From Scutellariae Radix Using Magnetic Molecularly Imprinted Polymers.Journal of separation science · 2026Article
- Gut-liver axis molecular mechanisms in alcohol-associated liver disease.Alcohol (Fayetteville, N.Y.) · 2026Review
- Baicalin: Natural Sources, Extraction Techniques, and Therapeutic Applications Against Bacterial Infections.Molecules (Basel, Switzerland) · 2025Review
- Exploring the therapeutic potential of baicalin against MCF-7 breast cancer cells: biochemical,Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
backgroundsAlcoholic liver disease (ALD), a consequence of excessive alcohol consumption, is characterized by high incidence and mortality rates. Presently, there are no effective pharmacological interventions available for the treatment of ALD. Baicalin (BA), a natural flavonoid derived from the root of Scutellaria baicalensis, has exhibited notable hepatoprotective effects. Nevertheless, the mechanisms through which BA influences the interaction between suppressor of cytokine signaling 1 (SOCS1) and macrophages during hepatic immune development remain insufficiently understood. MATERIALS AND
methodsThis study seeks to examine the regulatory effects of BA on ALD and to elucidate the relationship between SOCS1 and macrophage differentiation. Our experimental methodology involves the novel application of zebrafish as an in vivo model for ALD. To further investigate the underlying mechanisms, we employed gene knockout and overexpression techniques.
resultsThe study demonstrates that BA substantially alleviates ALD in both in vivo and in vitro settings by upregulating SOCS1 expression in macrophages. Furthermore, we elucidated the association between SOCS1 and macrophage reprogramming. Specifically, SOCS1 knockdown led to the downregulation of CD86, CD80, and iNOS expression, whereas SOCS1 overexpression enhanced the expression of CD206, CD163, IL-4, and IL-10.
conclusionIn conclusion, our findings suggest that BA attenuates ALD via the modulation of SOCS1-mediated macrophage reprogramming.
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