Ginsenoside CK Alleviates DSS-Induced IBD in Mice by Regulating Tryptophan Metabolism and Activating Aryl Hydrocarbon Receptor via Gut Microbiota Modulation

J Agric Food Chem. 2024 May 1;72(17):9867-9879. doi: 10.1021/acs.jafc.4c00245. Epub 2024 Apr 11.

Abstract

Dysbiosis of gut microbiota is believed to be associated with inflammatory bowel disease (IBD). Ginsenoside compound K (CK), the main metabolite of Panax ginseng ginsenoside, has proven effective as an anti-inflammatory agent in IBD. However, the mechanisms by which CK modulates gut microbiota to ameliorate IBD remain poorly understood. Herein, CK demonstrated the potential to suppress the release of proinflammatory cytokines by gut microbiota modulation. Notably, supplementation with CK promoted the restoration of a harmonious balance in gut microbiota, primarily by enhancing the populations of Lactobacillus and Akkermansia. Furthermore, CK considerably elevated the concentrations of tryptophan metabolites derived from Lactobacillus that could activate the aryl hydrocarbon receptor. Overall, the promising alleviative efficacy of CK primarily stemmed from the promotion of Lactobacillus growth and production of tryptophan metabolites, suggesting that CK should be regarded as a prospective prebiotic agent for IBD in the future.

Keywords: AhR; IBD; ginsenoside compound K; gut microbiota; inflammation; tryptophan metabolism.

MeSH terms

  • Animals
  • Bacteria / classification
  • Bacteria / drug effects
  • Bacteria / genetics
  • Bacteria / isolation & purification
  • Bacteria / metabolism
  • Dextran Sulfate* / pharmacology
  • Gastrointestinal Microbiome* / drug effects
  • Ginsenosides* / administration & dosage
  • Ginsenosides* / metabolism
  • Ginsenosides* / pharmacology
  • Humans
  • Inflammatory Bowel Diseases* / drug therapy
  • Inflammatory Bowel Diseases* / metabolism
  • Inflammatory Bowel Diseases* / microbiology
  • Male
  • Mice
  • Mice, Inbred C57BL*
  • Panax / chemistry
  • Panax / metabolism
  • Panax / microbiology
  • Receptors, Aryl Hydrocarbon* / genetics
  • Receptors, Aryl Hydrocarbon* / metabolism
  • Tryptophan* / metabolism

Substances

  • Dextran Sulfate
  • ginsenoside M1
  • Ginsenosides
  • Receptors, Aryl Hydrocarbon
  • Tryptophan