ArticleLaboratory investigation; a journal of technical methods and pathology2014
Tauroursodeoxycholic acid inhibits experimental colitis by preventing early intestinal epithelial cell death.
Article in Laboratory investigation; a journal of technical methods and pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 68 citations in OpenAlex.
- Clinical effects of ursodeoxycholic acid on patients with ulcerative colitis may improve via the regulation of IL-23-IL-17 axis and the changes of the proportion of intestinal microflora.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationTrial
- Microbiota-derived indole limitsScience advances · 2026Article
- Autophagy prevents ER stress-induced Tight Junction barrier disruption via claudin-2 homeostasis.bioRxiv : the preprint server for biology · 2026Article
- Bacteria enable tolerance to bile salt exposure in an immune-competent human intestinal model.Gut microbes · 2025Article
- Tauroursodeoxycholic Acid (TUDCA) Reduces ER Stress and Lessens Disease Activity in Ulcerative Colitis.medRxiv : the preprint server for health sciences · 2025Article
- Qing-Re-Hua-Shi Decoction ameliorates DSS-induced colitis by modulating multiple signaling pathways and remodeling the gut microbiota and metabolite profile.Frontiers in cellular and infection microbiology · 2025Article
- The role ofFrontiers in immunology · 2025Review
- Ursodeoxycholic and chenodeoxycholic bile acids attenuate systemic and liver inflammation induced by lipopolysaccharide in rats.Molecular and cellular biochemistry · 2025Article
- Protective effects of patchouli alcohol against DSS-induced ulcerative colitis.Scientific reports · 2024Article
- Harnessing nature's pharmacy: investigating natural compounds as novel therapeutics for ulcerative colitis.Frontiers in pharmacology · 2024Review
- Gut dysbiosis: Ecological causes and causative effects on human disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Exclusive Enteral Nutrition Exerts Anti-Inflammatory Effects through Modulating Microbiota, Bile Acid Metabolism, and Immune Activities.Nutrients · 2022Article
- Tauroursodeoxycholic Acid Inhibits Clostridioides difficile Toxin-Induced Apoptosis.Infection and immunity · 2022Article
- 5-Aminosalicylic acid ameliorates dextran sulfate sodium-induced colitis in mice by modulating gut microbiota and bile acid metabolism.Cellular and molecular life sciences : CMLS · 2022Article
- Tauroursodeoxycholic acid (TUDCA) improves intestinal barrier function associated with TGR5-MLCK pathway and the alteration of serum metabolites and gut bacteria in weaned piglets.Journal of animal science and biotechnology · 2022Article
- Tauroursodeoxycholic Acid Inhibits Nuclear Factor Kappa B Signaling in Gastric Epithelial Cells and Ameliorates Gastric Mucosal Damage in Mice.The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2022Article
- Defective humoral immunity disrupts bile acid homeostasis which promotes inflammatory disease of the small bowel.Nature communications · 2022Article
- Article
- Bile acids as inflammatory mediators and modulators of intestinal permeability.Frontiers in immunology · 2022Review
- Endoplasmic Reticulum Stress of Gut Enterocyte and Intestinal Diseases.Frontiers in molecular biosciences · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ulcerative colitis (UC) is characterized by increased epithelial cell death and subsequent breakdown of the intestinal epithelial barrier, which perpetuates chronic intestinal inflammation. Since fecal bile acid dysmetabolism is associated with UC and tauroursodeoxycholic acid (TUDCA) has been shown to improve murine colitis, we evaluated the effect of TUDCA on intestinal epithelial cell death in a mouse model of UC-like barrier dysfunction elicited by dextran sulfate sodium (DSS). We identified the prevention of colonic caspase-3 induction, a key proapoptotic marker which was also over-activated in UC, as the earliest event resulting in a clear clinical benefit. Whereas vehicle-treated mice showed a cumulative mortality of 40%, all TUDCA-treated mice survived the DSS experiment during a 14-day follow-up period. In line with a barrier protective effect, TUDCA decreased bacterial translocation to the spleen and stimulated mucin production. Similarly, TUDCA inhibited lipopolysaccharide-induced intestinal permeability and associated enterocyte apoptosis. The anti-apoptotic effect was confirmed in vitro by a dose-dependent inhibition of both receptor-dependent (using tumor necrosis factor and Fas ligand) and receptor-independent (staurosporine) caspase-3 induction in HT29 colonic epithelial cells. These data imply that caspase-3 activation is an early marker of colitis that is prevented by TUDCA treatment. These data, together with the previously reported beneficial effect in colitis, suggest that TUDCA could be an add-on strategy to current immunosuppressive treatment of UC patients.
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