Exp Mol Med.
2004 Dec;36(6):551-556.
Pseudolaric acid B induces apoptosis via activation of c-Jun N-terminal kinase and caspase-3 in HeLa cells
- Affiliations
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- 1China-Japan Research Institute of Medical Pharmaceutical Sciences ikejimat@vip.sina.com
- 2Department of Pharmacology Shenyang Pharmaceutical University Shenyang, 110016, China.
- 3Department of Clinical and Biomedical Sciences Showa Pharmaceutical University Tokyo 194-8543, Japan.
Abstract
- Pseudolaric acid B was isolated from Pseudolarix kaempferi Gordon (Pinaceae) and was evaluated for the anti-cancer effect in HeLa cells. We observed that pseudolaric acid B inhibited cell proliferation and induced apoptosis in a time- and dose-dependent manner. HeLa cells treated with pseudolaric acid B showed typical characteristics of apoptosis including the morphological changes and DNA fragmentation. JNK inhibitor, SP600125, markedly inhibited pseudolaric acid B-induced cell death. In addition, Bcl-2 expression was down-regulated while Bax protein level was up-regulated. Caspase-3 inhibitor, z-DEVD-fmk, partially blocked pseudolaric acid B-induced cell death, and the expression of two classical caspase substrates, PARP and ICAD, were both decreased in a time- dependent manner, indicative of downstream caspase activation.
Keyword
MeSH Terms
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Anthracenes/pharmacology
*Apoptosis
Caspases/antagonists & inhibitors/*metabolism
Cell Proliferation/drug effects
Cysteine Proteinase Inhibitors/pharmacology
Diterpenes/*pharmacology
Down-Regulation
Enzyme Activation
Hela Cells
Humans
JNK Mitogen-Activated Protein Kinases/drug effects/*metabolism
Oligopeptides/pharmacology
Protein Kinase Inhibitors/pharmacology
Proto-Oncogene Proteins c-bcl-2/metabolism
Signal Transduction/*drug effects
Up-Regulation
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