RRC ID |
72943
|
Author |
Yoshikawa M, Toyohara M, Ueda S, Shiroi A, Takeuchi H, Nishiyama T, Yamada T, Fukui H, Ishizaka S.
|
Title |
Glycyrrhizin inhibits TNF-induced, but not Fas-mediated, apoptosis in the human hepatoblastoma line HepG2.
|
Journal |
Biol Pharm Bull
|
Abstract |
To determine the transaminase-lowering action of glycyrrhizin (GL) immunologically, the effect of GL on tumor necrosis factor (TNF)-alpha- and Fas-mediated apoptosis was assessed using a human hepatoblastoma line, HepG2 cells. The HepG2 cells were resistant to TNF-alpha and anti-Fas antibody, but were rendered susceptible to TNF-alpha and anti-Fas antibody in the presence of actinomycin D (Act D), an inhibitor of RNA synthesis. The cytotoxicity induced by TNF-alpha/Act D or anti-Fas/Act D was accompanied by DNA fragmentation, indicating apoptotic death of HepG2 cells. GL partially prevented the apoptosis of HepG2 cells induced by TNF-alpha/Act D in a GL-dose dependent fashion. However, this protective effect of GL was not observed in the cytotoxicity of HepG2 caused by anti-Fas/Act D. Although the protection mechanism of GL, observed in a limited fashion against TNF-alpha-mediated apoptosis, is unclear, the present results provide an immunological explanation for the transaminase-lowering action of GL in the GL treatment of chronic liver diseases involving apoptotic hepatocyte death in their pathogenesis.
|
Volume |
22(9)
|
Pages |
951-5
|
Published |
1999-9-1
|
DOI |
10.1248/bpb.22.951
|
PMID |
10513619
|
MeSH |
Anti-Infective Agents / pharmacology*
Antibodies
Apoptosis*
Glycyrrhizic Acid / pharmacology*
Hepatoblastoma
Humans
Tumor Cells, Cultured
Tumor Necrosis Factor-alpha / antagonists & inhibitors
Tumor Necrosis Factor-alpha / physiology*
fas Receptor / immunology
fas Receptor / physiology*
|
IF |
1.863
|
Resource |
Human and Animal Cells |
Hep G2(RCB0459) |