20S-Protopanaxadiol-Induced Programmed Cell Death in Glioma Cells through Caspase-Dependent and -Independent Pathways

Guo-Yu Liu,†‡ Xuexian Bu,† Hang Yan,† and William W.-G. Jia*†‡
Department of Surgery and Brain Research Center, University of British Columbia, F233-2211 Wesbrook Mall, Vancouver, BC, V6T 2B5, Canada
J. Nat. Prod., 2007, 70 (2), pp 259–264
DOI: 10.1021/np060313t
Publication Date (Web): January 30, 2007
Copyright © 2007 American Chemical Society and American Society of Pharmacognosy
†

 Department of Surgery.

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‡

 Brain Research Center.

,
*

 Corresponding author. Tel:  604-822-0728. Fax:  604-322-0640. E-mail:  wjia@interchange.ubc.ca.

Abstract

Abstract Image

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.

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History

  • Published In Issue February 23, 2007
  • Received July 3, 2006

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