ArticleGastroenterology report2025
New Baitouweng Decoction alleviated DSS-induced colitis through the FXR/NLRP3 signaling pathway by regulating gut microbiota and bile acids.
Article in Gastroenterology report, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Dysregulated bile acid metabolism as a novel player in gout progression: emerging therapeutic strategies.Frontiers in endocrinology · 2025Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ulcerative colitis (UC) is a chronic disease that induces colon tissue damage. Previous studies have shown the clinical benefit of New Baitouweng Decoction (NBD). Here, we aimed to investigate the effects of NBD on dextran sodium sulfate (DSS)-induced UC and the underlying mechanisms in a mouse model. Methods: UC was induced in mice by using DSS for 7 days. The efficacy of NBD was determined by analysing the pathological appearance and the expression of inflammatory factors and tight junction proteins. 16S rDNA sequencing was used to describe the gut microbiota. Gas chromatography-mass spectrometry was employed to quantify bile acid (BA) levels. Spearman's correlation analysis was conducted to determine the relationship between gut microbiota composition and BA profiles. Western blot was used to detect the amounts of farnesoid X receptor (FXR), Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3), caspase-1, and cleaved caspase-1. Results: NBD reduced the disease activity index scores, ameliorated colonic pathological damage, inhibited colon inflammation, and repaired the intestinal barrier. In addition, 16S rDNA sequencing showed that NBD enhanced the relative abundance of beneficial bacteria such as Conclusion: NBD had a therapeutic effect on DSS-induced UC in a mouse model by regulating the gut microbiota, BAs, and subsequent FXR-NLRP3 pathway for decreasing the release of pro-inflammatory factors and repairing the intestinal barrier to preserve the equilibrium.
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