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Cytoprotective effect of tauroursodeoxycholate on hepatocyte apoptosis induced by peroxisome proliferator-activated

Michihiro Nonaka1, Susumu Tazuma, Hideyuki Hyogo

  • 1Department of Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.

Journal of Gastroenterology and Hepatology
|September 18, 2007
PubMed
Abstract

Insights

Tauroursodeoxycholate (TUDC) reduces troglitazone-induced apoptosis in liver cells, likely via the ERK pathway. This suggests TUDC may mitigate drug-induced liver toxicity.

Area of Science:

  • Hepatology
  • Molecular Biology
  • Pharmacology

Background:

  • Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands inhibit cancer cell growth and induce apoptosis.
  • Bile acids can induce hepatocyte apoptosis via nuclear receptor mechanisms.

Purpose of the Study:

  • To investigate the effect of two bile acids on PPARgamma-mediated growth inhibition.
  • To explore the role of the mitogen-activated protein kinase (MAPK) pathway in this interaction.

Main Methods:

  • Hepatocytes and hepatoma cells were treated with troglitazone (TGZ), a PPARgamma ligand.
  • Cells were pre-incubated with glycochenodeoxycholate (GCDC) or tauroursodeoxycholate (TUDC).
  • MAPK pathway phosphorylation (p38, JNK, ERK) was analyzed.

Main Results:

  • TGZ reduced cell viability and induced apoptosis.
  • GCDC enhanced TGZ-induced apoptosis, while TUDC attenuated it.
  • TUDC significantly enhanced ERK1/2 phosphorylation, an effect reversed by ERK inhibitors.

Conclusions:

  • TUDC exhibits anti-apoptotic and cytoprotective effects against TGZ-induced apoptosis.
  • The ERK signaling pathway is implicated in TUDC's protective mechanism.
  • TUDC may be a potential strategy to manage TGZ-induced hepatotoxicity.

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