Journal of ethnopharmacology · 2026
Babaodan ameliorates metabolic dysfunction-associated steatotic liver disease with co-modulation of FXR, NF-κB, and SLC22A7 in bile acid metabolism.
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Qiu Shi, Qiang Shifa, Wang Zhibo, Yang Lihua, Guo Sifan, Zeng Jiahan, Cai Ying, Lai Zhicheng, Xie Dandan, Che Li, Zhang Aihua
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: 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.
AIM OF THE STUDY: 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.
MATERIALS AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.
AIM OF THE STUDY: 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.
MATERIALS AND METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.