ArticleWorld journal of gastroenterology2025
Unveiling Xuanshen decoction: A novel approach to combat slow transit constipation.
Article in World journal of gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Article
- Gastrodin alleviates loperamide-induced slow transit constipation in mice by modulating the MAPK signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Therapeutic effects of three-strain probiotic combination on slow transit constipation: mechanistic insights into MAPK signaling pathway and gut microbiota restoration.Frontiers in pharmacology · 2025Article
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Authors and funding
5 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundXuanshen decoction (XSD) is a traditional Chinese medicine formulation that is often applied in treating slow transit constipation (STC). However, its specific therapeutic mechanism remains to be characterized.
aimTo investigate the mechanism of XSD for STC, we combined network pharmacology prediction, molecular docking analysis, and
methodsThe therapeutic effects of XSD on loperamide-induced STC in rats were assessed through 24-hour fecal number, fecal moisture content, and intestinal propelling rate. Hematoxylin-eosin and Alcian blue/periodic acid-Schiff staining were applied to analyze colonic mucosa for histopathological presentation and mucin production. Next, the mechanism of action of XSD for STC was elucidated through network pharmacology and molecular docking analyses, and the findings were validated by the animal experiments.
resultsXSD significantly alleviated the symptoms of STC in rats. Relative to the STC rats, in the medium-dose XSD and high-dose XSD rats, stem cell factor, C-kit, phospho-phosphoinositide 3-kinase/phosphoinositide 3-kinase, phospho-protein kinase B/protein kinase B, catalase, and superoxide dismutase were substantially upregulated (
conclusionXSD may inhibit oxidative-stress-induced apoptosis in interstitial cells of Cajal by stimulating the phosphoinositide 3-kinase/protein kinase B/nuclear factor erythroid 2-related factor 2 pathway, thereby effectively treating STC.
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