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Pithecellobium clypearia ameliorates ulcerative colitis through regulation of purine metabolism and gut microbiota

ABSTRACT:

Background: Pithecellobium clypearia (PC) is a traditional Chinese medicine with anti-inflammatory effects. However, the therapeutic efficacy and underlying mechanisms of PC in ulcerative colitis (UC) remain unclear.

Objective: This study applied an integrated microbiome-metabolomics approach to investigate PC’s pharmacological mechanisms against UC.

Materials and methods: A dextran sulfate sodium (DSS)-induced UC model was established, and the therapeutic efficacy of PC was evaluated using the disease activity index (DAI), histopathology, inflammatory cytokines, and tight junction proteins. Subsequently, 16S rRNA sequencing and metabolomics were performed to analyze alterations in the gut microbiota composition and colonic metabolic profiles.

Results: PC significantly ameliorated DSS-induced weight loss, reduced DAI scores, prevented colon shortening, and alleviated mucosal damage. Furthermore, PC decreased pro-inflammatory cytokines (TNF-α, IL-6, and IL-1β), increased anti-inflammatory IL-10, and restored ZO-1 and occludin expression. 16S rRNA sequencing showed PC restored gut dysbiosis, enriching beneficial Bacteroides while reducing pathogenic Escherichia-Shigella. Metabolomics indicated PC modulated colonic purine metabolism, normalizing key metabolites like xanthylic acid and aminoimidazole ribotide. Correlation analysis confirmed a strong crosstalk between these purine metabolites and specific gut microbiota.

Discussion and conclusions: PC ameliorates UC by suppressing inflammation and protecting the intestinal barrier. Its therapeutic mechanisms may be associated with the regulation of gut microbiota and host purine metabolism, providing a theoretical basis for future clinical applications.

INSTRUMENT(S): Liquid Chromatography MS - alternating - reverse-phase

PROVIDER: MTBLS14856 | MetaboLights | 2026-06-26

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS14856_LC-MS_alternating_reverse-phase.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS14856_LC-MS_alternating_reverse-phase_v2_maf.tsv	Tabular
	s_MTBLS14856.txt	Txt

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Project description:BACKGROUND: Ulcerative colitis (UC) is a chronic recurrent inflammatory disease of the gastrointestinal tract. Recent studies demonstrate that the phenolic tannin paeonol (Pae) attenuates UC in mouse models by downregulating inflammatory factors; however, molecular mechanisms linking the gut microbiota and microbial metabolism with Pae remain elusive. METHODS: The UC mouse model was induced using 3% dextran sodium sulfate (DSS). Clinical symptoms were assessed, hematoxylin-eosin staining were used to analyze the effect of Pae on pathological changes to mouse colons, and ELISA was used to evaluate inflammatory factor expression in the serum. Transmission electron microscopy and immunohistochemistry were used to examine the structure of the colonic epithelial barrier and its tight junction proteins. Potential mechanisms of Pae were explored by 16S rRNA-based gut microbiota analysis, fecal metabolomics and construction of a multiscale, multifactorial network. RESULTS: Pae treatment significantly reduced the weight loss and disease activity index, colon shortening, tissue damage, and changes in TNF-α, IL-1β, IL-6, and IL-4 cytokine levels. Conversely, Pae restored the integrity of the intestinal epithelial barrier by increasing the expression of Occludin and ZO-1. Pae also partially reverted the DSS-induced disturbance in intestinal flora composition by increasing the proportion of probiotic bacteria and inhibiting UC-associated dysregulation of gut microbiota metabolites such as bile acids (BA) and short chain fatty acids. Network analysis demonstrated that Lactobacillus was associated with increased levels of unbound BAs, which in turn were strongly associated with inflammatory factor levels. The results suggest that Pae influences BA synthesis by regulating hepatic FXR-SHP/LRH-1 and ileum FXR-FGF15 signaling pathways to maintain intestinal integrity in UC mice. CONCLUSION: Pae can alleviate DSS-induced UC in mice by restoring dysregulated intestinal microbiota and BA metabolism, which improves intestinal barrier function and colonic inflammation, thus suggesting a new mechanism for Pae treatment of UC.

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Pithecellobium clypearia ameliorates ulcerative colitis through regulation of purine metabolism and gut microbiota

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