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Bupleurum chinense DC polysaccharides ameliorate DSS-induced ulcerative colitis by regulating gut microbiota and tryptophan metabolism via NF-κB pathway

ABSTRACT:

Background: Bupleurum chinense DC polysaccharide (BCP) demonstrates a significant role in ameliorating gastric ulceration and enhancing intestinal barrier function, and have broad medicinal value. Nevertheless, the therapeutic effects and mechanisms in ulcerative colitis (UC) remain to be elucidated.

Purpose: The protective effect of BCP on dextran sulfate sodium (DSS)-induced UC and the related mechanisms will be discussed.

Methods: The efficacy of BCP was evaluated using a 2.5% DSS-induced UC model. The mechanistic contribution of the gut microbiota to the therapeutic efficacy of BCP in UC was elucidated through 16S rRNA sequencing, microbiota depletion experiment and fecal microbiota transplantation (FMT) experiments. Non-targeted metabolomics analysis was used to identify its potential metabolic pathways and core signaling pathways. In vitro, Caco-2 and NCM460 cells were treated with LPS to induce inflammation for assessing the effects of BCP.

Results: BCP significantly alleviated UC injuries, including decreasing body weight loss and disease activity index (DAI), and increasing colon length. Moreover, BCP significantly reduced inflammatory cytokine levels and improved histopathological damage in the colon. BCP promoted tight junction proteins (TJ proteins) expression, facilitated MUC2 secretion, and helped alleviate DSS-induced intestinal barrier damage. BCP could improve the gut microbiota changes, and BCP’s therapeutic effects on UC were mediated through the gut microbiota in vivo experiment. Additionally, metabolomics analysis revealed that BCP could impact the tryptophan metabolism pathway and target the AHR-NF-κB signaling pathway to improve UC.

Conclusion: This study reveals that BCP improves UC through modulation of the gut microbiota and the tryptophan metabolism via NF-κB axis.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS13814 | MetaboLights | 2026-02-01

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS13814_LC-MS_negative_reverse-phase_metabolite_profiling.txt	Txt
	a_MTBLS13814_LC-MS_positive_reverse-phase_metabolite_profiling.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS13814_LC-MS_negative_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular
	m_MTBLS13814_LC-MS_positive_reverse-phase_metabolite_profiling_v2_maf.tsv	Tabular

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Project description:Background: Ulcerative colitis (UC) is a significant and challenging condition in the digestive system, necessitating the development of effective therapeutic interventions. The Daifu decoction (DFD) is derived from the Lizhong decoction, a classic traditional Chinese Medicine (TCM) formula used to treat digestive diseases. Previous studies have found that DFD has a clear therapeutic effect on UC. This study aimed to investigate the underlying mechanisms of DFD in UC treatment.Methods: A mouse model of dextran sulfate sodium (DSS)-induced UC was established, and mice were treated with DFD using the concentrations 1.6 g/kg/d, 3.2 g/kg/d, and 6.4 g/kg/d for 7 days. H&E and AB-PAS staining, ELISA, qPCR, and immunofluorescence were selected to assess the role of DFD in alleviating colitis and improving intestinal barrier damage. In addition, untargeted metabolomics and transcriptomics helped investigate the potential mechanism of DFD against UC, 16S rRNA sequencing evaluated the characteristics of the gut microbiota. The key target and downstream molecules were verified by molecular docking, molecular dynamics simulation, qPCR, western blotting, and immunohistochemistry.Results: DFD prevented goblet cell loss, downregulated proinflammatory factors in serum, and improved tight junction mRNA and protein expression in colon tissue. Furthermore, DFD decreased the proportion of pathogenic microbes, while increasing the microbiota diversity and the proportion of beneficial bacterial. The integrated multi-omics analysis revealed that PRKCG was the key target of DFD to improve UC. Molecular docking and molecular dynamics simulations further confirmed that the active components of DFD could bind to PRKCG stably. The results of qPCR, western blotting, and immunohistochemistry revealed that DFD could regulate PKCγ/ERK/NF-κB pathway.Conclusion: DFD can exert therapeutic effects on UC by regulating the PKCγ/ERK/NF-κB signaling pathway and the gut microbiota to restore the intestinal barrier and decrease the secretion of proinflammatory cytokines.

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Bupleurum chinense DC polysaccharides ameliorate DSS-induced ulcerative colitis by regulating gut microbiota and tryptophan metabolism via NF-κB pathway

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