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Updated: Jul 16, 2026

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In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
Published on: October 19, 2018
Hepatocyte tight-junctional permeability is increased in rat experimental colitis
1Department of Internal Medicine, University of Padova, Italy.
Gastroenterology
|October 10, 1997
Summary
Inflammatory bowel disease (IBD) causes liver injury due to increased intestinal toxin translocation. This study found increased hepatocyte tight junction permeability in experimental IBD, contributing to liver complications.
Area of Science:
- Gastroenterology
- Hepatology
- Cell Biology
Background:
- Hepatobiliary complications are observed in inflammatory bowel disease (IBD).
- Intestinal toxin translocation via compromised hepatocyte tight junctions may cause these complications.
Purpose of the Study:
- To investigate the role of tight junctions in the pathogenesis of hepatobiliary complications in experimental IBD.
Main Methods:
- Colitis induced in rats using trinitrobenzene sulfonic acid.
- Hepatocellular tight junction function assessed via horseradish peroxidase and lanthanum permeability assays in perfused livers.
- Immunofluorescence used to examine cingulin and ZO-1 localization in hepatocyte junctions.
Main Results:
- Colitis increased serum bilirubin and bile acid levels.
- A 2.5-fold increase in paracellular horseradish peroxidase biliary excretion and a ninefold increase in lanthanum permeability were observed.
- Liver histology and tight junction protein localization remained similar to normal controls.
Conclusions:
- Experimental colitis leads to hepatobiliary complications with increased hepatocyte tight junction permeability.
- Subtle alterations in tight junction function may contribute to liver injury in IBD.
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