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Published on: October 13, 2023
20(S/R)-Ginsenoside Rh1 Alleviates AOM/DSS-Induced Colorectal Cancer: Gut-Microbiota Modulation and
Linqian Lu1,2, Jinyu Min1, Yansong Gao2
1School of Pharmaceutical Sciences, Changchun University of Chinese Medicine, Changchun 130117, China.
Abstract:
Colorectal cancer (CRC) is intricately linked to gut microbiota dysbiosis and tryptophan (Trp) metabolic dysregulation. This study aimed to clarify the role and mechanisms of 20(S/R)-ginsenoside Rh1 in suppressing colorectal cancer through the regulation of gut microbiota and Trp metabolism. Azoxymethane/dextran sulfate sodium (AOM/DSS)was employed to induce a CRC mouse model, followed by treatment with 20(S/R)-ginsenoside Rh1 at 100 mg·kg-1·day-1 for 6 weeks. 20(S/R)-ginsenoside Rh1 significantly reduced the disease activity index (DAI) score, restored colon length, and decreased tumor count. 20(S/R)-Ginsenoside Rh1 ameliorated gut dysbiosis by increasing gut microbial diversity and elevating the prevalence of beneficial bacteria, including Lactobacillus, and stimulated the production of indole derivatives, including indole-3-propionic acid (IPA), indole-3-acetic acid (IAA), and indole-3-lactic acid (ILA) by enriching Trp -metabolizing bacteria such as Lactobacillus reuteri. These changes further activated the AhR/CYP1A1/IL-22 and PXR/TLR4 pathways, upregulated the expression of intestinal tight junction proteins, suppressed the secretion of proinflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IFN-γ, and elevated the levels of the anti-inflammatory cytokine IL-10. Furthermore, 20(S/R)-ginsenoside Rh1 reduces the serum kynurenine (Kyn)/Trp ratio, downregulates the expression of forkhead box P3 (FoxP3), a marker of regulatory T (Treg) cells, and increases the number of CD8+ T cells by inhibiting the expression of indoleamine 2,3-dioxygenase 1 (IDO1) in colonic tissue. In conclusion, 20(S/R)-ginsenoside Rh1 showed potential anti-CRC activity, with our study observing links between its action and gut microbiota structure regulation, Trp metabolism modulation, AhR/PXR-mediated intestinal barrier activation, and IDO1-related immune suppression reversal.
Insights
20(S/R)-ginsenoside Rh1 combats colorectal cancer by modulating gut microbiota and tryptophan metabolism. It restores gut health, activates protective pathways, and reverses immune suppression, showing potential as an anti-CRC agent.
Area of Science:
- Microbiology
- Pharmacology
- Immunology
Background:
- Colorectal cancer (CRC) is linked to gut microbiota dysbiosis and tryptophan (Trp) metabolism disruption.
- Understanding the mechanisms of natural compounds in CRC prevention is crucial.
Purpose of the Study:
- To investigate the anti-CRC effects of 20(S/R)-ginsenoside Rh1.
- To elucidate its mechanisms involving gut microbiota and Trp metabolism.
Main Methods:
- A mouse model of CRC was induced using Azoxymethane/dextran sulfate sodium (AOM/DSS).
- Mice were treated with 20(S/R)-ginsenoside Rh1 (100 mg·kg-1·day-1 for 6 weeks).
- Analyses included disease activity index, colon length, tumor count, gut microbiota composition, Trp metabolites, and immune markers.
Main Results:
- 20(S/R)-ginsenoside Rh1 reduced CRC severity, restored colon length, and decreased tumor burden.
- It ameliorated gut dysbiosis, increased microbial diversity, and promoted beneficial bacteria like *Lactobacillus*.
- It stimulated indole derivative production, activated AhR/CYP1A1/IL-22 and PXR/TLR4 pathways, enhanced intestinal barrier function, and modulated immune responses by inhibiting IDO1 and reversing Treg cell markers.
Conclusions:
- 20(S/R)-ginsenoside Rh1 exhibits significant anti-CRC activity.
- Its efficacy is linked to regulating gut microbiota structure and Trp metabolism.
- It activates intestinal barrier pathways and reverses IDO1-mediated immune suppression.
