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Effect of ginsenoside compound K on alleviating colitis via modulating gut microbiota


ABSTRACT:

Background

Ginsenoside compound K (GC-K) potentially alleviates ulcerative colitis involved in gut microbiota, which is significantly associated with the occurrence and development of colitis. However, the effect and mechanism of GC-K on anti-colitis in relation to gut microbiota are not clear. This study focused on the prevention and mechanism of GC-K on Dextran sulfate sodium (DSS)-induced colitis of mice pertinent to gut microbiota.

Methods

DSS was used to establish a chronic colitis mouse model. Body weight analysis, colon length measurement, HE staining, and inflammatory factors levels were processed in animal experiments. Flow cytometry was employed to analyze Th17/Treg cells in the mouse spleen and blood. 16S rRNA sequencing was utilized to analyze gut microbiota. Fecal microbiota transplantation (FMT) experiment was employed to verify the anti-colitis efficacy of GC-K by reshaping gut microbiota.

Results

GC-K significantly relieved colitis-related symptoms due to decreased disease activity index (DAI) scores, spleen weight, and increased colon length. Additionally, the tight junction proteins were increased, and the pro-inflammatory cytokines, such as TNF-α, IL-6, IL-1β and IL-17, were decreased after GC-K treatment. Furthermore, Bacteroides spp. significantly increased after modeling. Moreover, FMT experiments confirmed that GC-K-driven gut microbiota greatly relieved DSS-induced colitis.

Conclusion

GC-K alleviated colitis via the modulation of gut microbiota.

Graphical Abstract

Supplementary Information

The online version contains supplementary material available at 10.1186/s13020-022-00701-9. Highlights Ginsenoside Compound K (GC-K) alleviated colitis in DSS-induced Mice. GC-K modulated gut microbiota in DSS-induced mice. GC-K relieved colitis via regulating gut microbiota. GC-K-driven gut microbial effectively ameliorated colitis.

Supplementary Information

The online version contains supplementary material available at 10.1186/s13020-022-00701-9.

SUBMITTER: Wang L 

PROVIDER: S-EPMC9795722 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature

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