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KMID : 0811719970010010107
Korean Journal of Physiology & Pharmacology
1997 Volume.1 No. 1 p.107 ~ p.115
Induction of Apoptosis by Bile Acids in HepG2 Human Hepatocellular Carcinoma Cells
Jin Hyen Baek
Jung-Ae Kim/Chang-Mo Kang/Yong Soo Lee/Kyu-Won Kim
Abstract
We studied the effects of bile acids on the induction ofapoptosis 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 A23l87 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.
KEYWORD
Intracellular Ca2£«, Apoptosis, Bile acids, HepG2 cells,
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