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Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
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Related Experiment Video

Updated: Jan 24, 2026

A Small Animal Model of Ex Vivo Normothermic Liver Perfusion
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Tauroursodeoxycholate protects from glycochenodeoxycholate-induced gene expression changes in perfused rat liver.

Martha Paluschinski1, Mirco Castoldi1, David Schöler1

  • 1Clinic for Gastroenterology, Hepatology and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Moorenstraße 5, 40225 Düsseldorf, Germany.

Biological Chemistry
|June 2, 2019
PubMed
Summary

Tauroursodeoxycholate (TUDC) protects rat livers from glycochenodeoxycholate (GCDC)-induced damage. TUDC counteracts GCDC

Keywords:
GCDCTUDCliver protectionmiRNAβ1-integrin

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Area of Science:

  • Hepatology
  • Molecular Biology
  • Toxicology

Background:

  • Tauroursodeoxycholate (TUDC) is known to protect rat hepatocytes from glycochenodeoxycholate (GCDC)-induced apoptosis.
  • The protective mechanisms of TUDC against GCDC-induced cellular stress, particularly concerning gene expression, require further elucidation.

Purpose of the Study:

  • To investigate the protective effects of TUDC against GCDC-induced hepatotoxicity by analyzing gene expression modulation.
  • To identify specific molecular pathways influenced by GCDC and TUDC in rat liver perfusion models.

Main Methods:

  • Gene array-based transcriptome analysis and quantitative polymerase chain reaction (qPCR) on rat liver RNA.
  • Perfusion of rat livers with GCDC and TUDC (20 μm for 2 h) to assess gene expression and cellular damage markers like lactate dehydrogenase (LDH).

Main Results:

  • GCDC induced significant LDH release and upregulated pro-inflammatory genes, oxidative stress markers (8OH(d)G), and pro-apoptotic microRNAs (miR-15b/16).
  • TUDC co-perfusion prevented LDH release and counteracted GCDC-induced changes in pro-inflammatory genes.
  • TUDC upregulated pro-proliferative and anti-apoptotic p53 target genes (p53, p21) and prevented the GCDC-induced downregulation of miR-15b/16 target genes.

Conclusions:

  • TUDC exhibits hepatoprotective effects by modulating GCDC-induced gene expression changes in rat livers.
  • TUDC counteracts GCDC-induced inflammation, oxidative stress, and apoptosis, while promoting pro-proliferative and anti-apoptotic pathways.