ArticleJournal of pharmaceutical analysis2025
Phillygenin ameliorates tight junction proteins reduction, fibrosis, and apoptosis in mice with chronic colitis via TGR5-mediated PERK-eIF2α-Ca
Article in Journal of pharmaceutical analysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Dysregulated bile acid metabolism impairs intestinal barrier integrity via defective GPBAR1 signaling in low-birth-weight suckling piglet.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2026Article
- Phillygenin, a Plant-Derived Lignan, Attenuates Renal Inflammation, Fibrosis, and Pyroptosis in a Unilateral Ureteral Obstruction Model.Nutrients · 2026Article
- Mechanisms and therapeutic potential of traditional Chinese medicine for inflammatory bowel disease.World journal of gastroenterology · 2026Review
- Using the Phillygenin Ameliorates the Severe Acute Pancreatitis in Rats by Inhibiting TLR4/NF-κB Pathway.Journal of inflammation research · 2026Article
- Endosome-phagophore linking assemblies for the degradation of membrane/extracellular proteins.Nature communications · 2025Article
- Pinoresinol enhances oral barrier integrity and function in human buccal cell monolayers.PloS one · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Ulcerative colitis (UC) is an idiopathic, relapsing, and etiologically complicated chronic inflammatory bowel disease. Despite substantial progress in the management of UC, the outcomes of mucosal barrier repair are unsatisfactory. In this study, phillygenin (PHI) treatment alleviated the symptoms of chronic colitis in mice, including body weight loss, severe disease activity index scores, colon shortening, splenomegaly, oxidative stress, and inflammatory response. In particular, PHI treatment ameliorated the tight junction proteins (TJs) reduction, fibrosis, apoptosis, and intestinal stem cell activity, indicating that PHI exerted beneficial effects on the intestinal mucosal barrier in mice with chronic colitis. In the NCM460 cells damage model, dextran sulfate sodium triggered the sequential induction of TJs reduction, fibrosis, and apoptosis. Takeda G protein-coupled receptor-5 (TGR5) dysfunction mediated NCM460 cell injury. Moreover, PHI treatment enhanced TJs and suppressed fibrosis and apoptosis to maintain NCM460 cell function, depending on TGR5 activation. PHI promoted TGR5 activation and elevated intracellular cyclic adenosine monophosphate levels in HEK 293T cells transfected with TGR5 expression plasmids. Cellular thermal shift assay and molecular docking studies confirmed that PHI directly binds to TGR5, indicating that PHI is an agonist of TGR5. The process of PERK-eIF2α pathway-mediated endoplasmic reticulum Ca
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Registered trials
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