Babaodan Ameliorates Metabolic Dysfunction-Associated Steatotic Liver Disease with Co-Modulation of FXR, NF-κB, and SLC22A7 in Bile Acid Metabolism.

Authors

Shi Qiu, Shifa Qiang, Zhibo Wang, Lihua Yang, Sifan Guo, Jiahan Zeng, Ying Cai, Zhicheng Lai, Dandan Xie, Li Che, Aihua Zhang

Published in

Journal of ethnopharmacology. Pages 122201. Jul 19, 2026. Epub Jul 19, 2026.

Abstract

Babaodan (BBD) is a traditional Chinese medicinal formula originating from a Ming Dynasty prescription. It has long been clinically applied in China for liver disorders, yet its systemic mechanism against metabolic dysfunction-associated steatotic liver disease (MASLD) remains poorly understood.
To decipher the multi-target mechanism by which BBD ameliorates MASLD, with a focus on the integration of bile acid homeostasis and inflammatory signaling, and to identify the key therapeutic axis underlying its hepatoprotective effects.
A multi-omics approach was employed, combining single-cell transcriptomics of MASLD mouse livers, untargeted serum metabolomics, targeted liver proteomics of bile acid metabolism-related proteins, and network-based integrative analysis. Functional validation was performed in palmitic acid-treated AML12 hepatocytes and a high-fat diet-induced mouse MASLD model. Western blotting and biochemical assays assessed key pathway components and biomarkers.
Single-cell transcriptomics identified hepatocytes as the principal hub where bile acid disruption and NF-κB-driven inflammation accumulation, with FXR as a central dysregulated node. BBD dose-dependently alleviated hepatocyte steatosis, apoptosis, and inflammation. Serum metabolomics showed BBD normalized 17 of 24 MASLD-associated metabolites, with bile acid biosynthesis as the most restored pathway. Targeted proteomics revealed coordinated regulation of bile secretion-related proteins, and multi-omics network analysis identified SLC22A7 as a central hub correlated with bilirubin, insulin, and inflammatory mediators. Functional validation confirmed that BBD treatment was associated with upregulation of FXR and SLC22A7, suppression of NF-κB p65 phosphorylation, and reduction of IL-6, identifying these molecules as interconnected features of the therapeutic response.
BBD alleviates MASLD via co-modulation of the FXR, NF-κB, and SLC22A7, restoring bile acid homeostasis and reducing inflammation. These findings reveal BBD as a multi-target agent and provide support for its clinical application in MASLD.

PMID:
42472598
Bibliographic data and abstract were imported from PubMed on 20 Jul 2026.

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