# Combined Prebiotic Extract of Mung Bean, Red Bean, and Fennel Improves Intestinal Barrier Integrity in HT-29 Cells and DSS-Induced Colitis via Gut Microbiota Alteration

**Authors:** Chul Sang Lee, Woo-Young Jang, Ju-Yeon Kim, Myung-Hyun Lee, Sung-Joon Mo, Yong-Tae Kim, Jae-Jung Shim, Jae-Hwan Lee

PMC · DOI: 10.3390/cimb48010032 · Current Issues in Molecular Biology · 2025-12-26

## TL;DR

A prebiotic extract from mung bean, red bean, and fennel improves gut health by reducing inflammation and supporting the intestinal barrier in cells and a mouse model of colitis.

## Contribution

The study demonstrates a novel prebiotic extract's ability to modulate gut microbiota and enhance intestinal barrier integrity in inflammatory conditions.

## Key findings

- PME reduced inflammation and improved intestinal barrier markers in LPS-stimulated HT-29 cells.
- PME alleviated colitis symptoms in mice by modulating gut microbiota and reducing inflammatory cytokines.
- PME increased beneficial gut bacteria and suppressed harmful taxa in a DSS-induced colitis model.

## Abstract

Inflammatory bowel disease (IBD) involves chronic inflammation and disruption of the intestinal barrier, often accompanied by alterations in gut microbiota composition. This study examined the protective potential of a prebiotic mixture extract (PME) prepared from Vigna radiata (mung bean), Vigna angularis (red bean), and Foeniculum vulgare (fennel) using the HT-29 cell and colitis animal model. PME exhibited concentration-dependent antioxidant activity, with greater radical-scavenging capacity in the ABTS assay than in the DPPH assay. In LPS-stimulated HT-29 epithelial cells, PME reduced the mRNA expression of inflammation-associated genes (TNF-α, IL-1β, NF-κB) and upregulated tight junction markers (CLDN1 and OCLN), demonstrating its anti-inflammatory and supportive effects on the intestinal barrier. Vitexin, a C-glycosylated flavonoid, was detected in PME and is expected to mediate these protective effects. In a DSS-induced colitis mouse model, PME administration alleviated disease severity by increasing colon length, reducing serum levels of inflammatory cytokines and COX-2/PGE2, and restoring intestinal permeability. Furthermore, PME modulated the gut microbiota by enhancing beneficial bacteria such as Bifidobacterium and Faecalibaculum while suppressing inflammation-associated taxa, including Escherichia, Bacteroides, and Mucispirillum. These improvements collectively suggest that PME reinforces epithelial barrier integrity and promotes intestinal homeostasis through both anti-inflammatory and microbiota-regulating actions.

## Linked entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124], IL1B (interleukin 1 beta) [NCBI Gene 3553], NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790], CLDN1 (claudin 1) [NCBI Gene 9076], OCLN (occludin) [NCBI Gene 100506658], COX2 (cytochrome c oxidase subunit II) [NCBI Gene 4513]
- **Chemicals:** vitexin (PubChem CID 5280441)
- **Diseases:** inflammatory bowel disease (MONDO:0005265), colitis (MONDO:0005292)
- **Species:** Vigna radiata (taxon 157791), Vigna angularis (taxon 3914), Bifidobacterium (taxon 1678), Faecalibaculum (taxon 1729679), Escherichia (taxon 561), Bacteroides (taxon 816), Mucispirillum (taxon 248038)

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12839834/full.md

## References

61 references — full list in the complete paper: https://tomesphere.com/paper/PMC12839834/full.md

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Source: https://tomesphere.com/paper/PMC12839834