ArticleWorld journal of gastroenterology2025
Kangfuxin solution alleviates esophageal stenosis after endoscopic submucosal dissection: A natural ingredient strategy.
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 4 papers.
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Who cites it
4 citing papers in PubMed.
- Therapeutic potential ofPharmaceutical biology · 2026Review
- Study on the mechanism of action of Kangfuxin liquid in alleviating DSS-induced ulcerative colitis in mice.Frontiers in pharmacology · 2026Article
- Chinese patent medicine: Opening new perspectives for treatment of post-endoscopic submucosal dissection esophageal stricture in esophageal cancer patients.World journal of gastroenterology · 2025Article
- Rising of natural therapies: Potential and challenges of traditional Chinese medicine in the management of gastrointestinal diseases.World journal of gastroenterology · 2025Article
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10 authors.
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Abstract
backgroundEsophageal stricture ranks among the most significant complications following endoscopic submucosal dissection (ESD). Excessive fibrotic repair is a typical pathological feature leading to stenosis after ESD.
aimTo examine the effectiveness and underlying mechanism of Kangfuxin solution (KFX) in mitigating excessive fibrotic repair of the esophagus post-ESD.
methodsPigs received KFX at 0.74 mL/kg/d for 21 days after esophageal full circumferential ESD. Endoscopic examinations occurred on days 7 and 21 post-ESD.
resultsCompared to the Control group, the groups treated with KFX and prednisolone exhibited reduced esophageal stenosis, lower weight loss rates, and improved food tolerance 21 d after ESD. After treatment, Masson staining revealed thinner and less dense collagen fibers in the submucosal layer. Additionally, the expression of fibrotic effector molecules was notably inhibited. Mechanistically, KFX downregulated the transduction levels of fibrotic functional molecules such as TGF-β1, Smad2/3, and p-Smad2/3.
conclusionKFX showed promise as a therapeutic option for post-full circumferential esophageal ESD strictures, potentially by suppressing fibroblast fibrotic activity through modulation of the TGF-β1/Smads signaling pathway.
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