20S-protopanaxadiol-induced programmed cell death in glioma cells through caspase-dependent and -independent pathways.

Keywords
  • cysteine proteinases
  • biochemical pathways
  • apoptosis
  • Panax ginseng
  • sapogenins
  • saponins
  • triterpenoids
  • cytotoxicity
  • cultured cells
  • humans
  • anticarcinogenic activity
  • caspases
  • 20S-Protopanaxadiol
PISSN
0163-3864
Publication Dbxref
PMID:17261067
Title
20S-protopanaxadiol-induced programmed cell death in glioma cells through caspase-dependent and -independent pathways.
Publication Type
Journal Article
Additional Publication Type(s)
Research Support, Non-U.S. Gov't
Series Name
Journal of natural products
Volume
70
Publication Year
2007
Issue
2
Page Numbers
259-64
Journal Abbreviation
J Nat Prod
Publication Date
2007 Feb
Citation
Liu GY, Bu X, Yan H, Jia WW. 20S-protopanaxadiol-induced programmed cell death in glioma cells through caspase-dependent and -independent pathways.. Journal of natural products. 2007 Feb; 70(2):259-64.
ISSN
0163-3864
Language Abbr
eng
Publication Model
Print-Electronic
Authors
Liu GY, Bu X, Yan H, Jia WW
Language
English
Journal Country
United States
Abstract

20S-Protopanaxadiol (1) is an aglycon metabolic derivative of the protopanaxadiol-type ginseng saponins. In the present study, 1 was used to induce cytotoxicity for two human glioma cell lines, SF188 and U87MG. For the SF188 cells, 1 activated caspases-3, -8, -7, and -9 within 3 h and induced rapid apoptosis, which could be partially inhibited by a general caspase blocker and completely abolished when the caspase blocker was used in combination with an antioxidant. Compound 1 also induced cell death in U87MG cells but did not activate any caspases in these cells. Monodansylcadaverine staining showed that 1 induced dramatic autophagy in both cell lines. Elevated levels of superoxide anion in both cells and reduced levels of phosphorylated Akt in U87MG cells were also demonstrated. These results showed that 20S-protopanaxadiol (1) induces different forms of programmed cell death, including both typical apoptosis and autophagy through both caspase-dependent and -independent mechanisms.

Database Reference Annotations
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