ArticleBioMed research international2019
GYY4137 Attenuates Sodium Deoxycholate-Induced Intestinal Barrier Injury Both In Vitro and In Vivo.
Article in BioMed research international, 2019. 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, 11 citations in OpenAlex.
- Article
- Effect of H2S on endothelial barrier function impairment in anorectal vascular plexus caused by deoxycholic acid.Frontiers in medicine · 2025Article
- [α-Cyperone Antagonizes Intestinal Mucosal Inflammatory Response Through Modulation of TLR4/NF-κB Signaling Pathway to Alleviate Crohn's Disease-Like Colitis in Mice].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Article
- GYY4137, as a slow-releasing HFrontiers in pharmacology · 2024Article
- Recent Development of the Molecular and Cellular Mechanisms of Hydrogen Sulfide Gasotransmitter.Antioxidants (Basel, Switzerland) · 2022Review
- Bile acid detergency: permeability, inflammation, and effects of sulfation.American journal of physiology. Gastrointestinal and liver physiology · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesSubstantial studies have demonstrated that an elevated concentration of deoxycholic acid (DCA) in the colonic lumen may play a critical role in the pathogenesis of intestinal barrier dysfunction and inflammatory bowel disease (IBD). The purpose of this study was to investigate the protective effects of GYY4137, as a novel and synthetic H
methodsIn this study, Caco-2 monolayers and mouse models with high SDC concentration in the lumen were used to study the effect of GYY4137 on intestinal barrier dysfunction induced by SDC and its underlying mechanisms.
resultsIn Caco-2 monolayers, a short period of addition of SDC increased the permeability of monolayers obviously, changed distribution of tight junctions (TJs), and improved the phosphorylation level of myosin light chain kinase (MLCK) and myosin light chain (MLC). However, pretreatment with GYY4137 markedly ameliorated the SDC-induced barrier dysfunction. Being injected with GYY4137 could enable mice to resist the SDC-induced injury of the intestinal barrier. Besides, GYY4137 promoted the recovery of the body weight and intestinal barrier histological score of mice with the gavage of SDC. GYY4137 also attenuated the decreased expression level of TJs in mice treated with SDC.
conclusionTaken together, this research suggests that GYY4137 preserves the intestinal barrier from SDC-induced injury via suppressing the activation of P-MLCK-P-MLC2 signaling pathway and increasing the expression level of tight junctions.
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