Korean J Physiol Pharmacol.  1997 Feb;1(1):107-115.

Induction of apoptosis by bile acids in HepG2 human hepatocellular carcinoma cells

Affiliations
  • 1Department of Molecular Biology, Pusan National University, Pusan 609-735 South Korea.
  • 2Department of Biology, Pusan National University, Pusan 609-735 South Korea.
  • 3Department of Physiology, College of Medicine, Kwandong University, Kangnung 210-701, South Korea.

Abstract

We studied the effects of bile acids on the induction of apoptosis in HepG2 human hepatocellular carcinoma cells. Treatment with either ursodeoxycholic acid (UDCA) or lithocholic acid (LCA) resulted in a dose- and time-dependent decrease in cell viability assessed by MTT assay. Both UDCA and LCA also induced genomic DNA fragmentation, a hallmark of apoptosis, indicating that the mechanism by which these bile acids induce cell death was through apoptosis. Cycloheximide, a protein synthesis inhibitor, blocked the apoptosis induced by these bile acids, implying that new protein synthesis may be required for the apoptosis. Intracellular Ca2+ release blockers (dantrolene and 3,4,5-trimethoxybenzoic acid-8-(diethylamino)octyl ester) inhibited decreased cell viability and DNA fragmentation induced by these bile acids. Treatment of HepG2 cells with calcium ionophore A23187 induced DNA fragmentation. These results suggest that UDCA and LCA induce apoptosis in the HepG2 cells and that the activation of intracellular Ca2+ signals may play an important role in the apoptosis induced by these bile acids.


MeSH Terms

Apoptosis*
Bile Acids and Salts*
Bile*
Calcimycin
Calcium
Carcinoma, Hepatocellular*
Cell Death
Cell Survival
Cycloheximide
DNA Fragmentation
Hep G2 Cells
Humans*
Lithocholic Acid
Ursodeoxycholic Acid
Bile Acids and Salts
Calcimycin
Calcium
Cycloheximide
Lithocholic Acid
Ursodeoxycholic Acid
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