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Astragalus Polysaccharide Enhances Voriconazole Metabolism under Inflammatory Conditions through the Gut Microbiota

Xiaokang Wang1,2,3, Xianjing Hu2,4, Chunxiao Ye5

  • 1The Marine Biomedical Research Institute of Guangdong Zhanjiang, Zhanjiang, Guangdong, China.

Journal of Clinical and Translational Hepatology
|May 23, 2024
PubMed
Abstract

Insights

Astragalus polysaccharide (APS) enhances voriconazole (VRC) metabolism and reduces liver damage by increasing Bifidobacterium bifidum, which modulates the gut-liver axis and CYP2C19 expression.

Area of Science:

  • Pharmacology and Toxicology
  • Microbiology and Immunology
  • Hepatology

Background:

  • Voriconazole (VRC) is a crucial antifungal agent associated with significant hepatotoxicity.
  • Astragalus polysaccharide (APS) has shown potential in regulating VRC metabolism and mitigating liver injury.
  • The precise mechanism of APS in VRC metabolism remains to be elucidated.

Purpose of the Study:

  • To investigate the underlying mechanism by which APS influences VRC metabolism.
  • To explore the role of gut microbiota, specifically Bifidobacterium bifidum, in APS-mediated VRC metabolism regulation.
  • To determine the impact of APS on VRC-induced hepatotoxicity via the gut-liver axis.

Main Methods:

  • Assessed VRC-hepatotoxicity association using the Roussel Uclaf Causality Assessment Method scale.
  • Conducted in vitro and in vivo experiments on a lipopolysaccharide-induced rat inflammation model.
  • Utilized cytokine profiling, immunohistochemistry, qPCR, metabolite analysis, drug concentration measurements, intestinal biodiversity analysis, and Bifidobacterium bifidum replenishment.

Main Results:

  • APS did not directly affect hepatocytes but significantly increased Bifidobacterium bifidum abundance.
  • APS induced an anti-inflammatory response in the liver, indirectly enhancing VRC metabolism.
  • APS inhibited pro-inflammatory mediator secretion and reduced inhibition of CYP2C19 transcription via the NF-κB pathway.

Conclusions:

  • APS alleviates VRC-induced liver damage through immunomodulatory effects on hepatic tissues.
  • APS indirectly regulates VRC-metabolizing enzyme CYP2C19 expression via the gut-liver axis.
  • The findings highlight the therapeutic potential of APS in managing VRC-associated hepatotoxicity.
Keywords:
Anti-inflammatory responsesAstragalus polysaccharideBifidobacterium bifidumGut MicrobiotaHepatotoxicityMetabolismRUCAMVoriconazole

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