Proapoptotic Ginsenosides Compound K and Rh2 Enhance Fas-induced Cell Death of Human Astrocytoma Cells Through Distinct Apoptotic Signaling Pathways / Journal of the Korean Cancer Association, 대한암학회지
Cancer Research and Treatment
;
: 36-44, 2009.
Article
in English
| WPRIM
| ID: wpr-17146
ABSTRACT
PURPOSE:
Malignant astrocytomas are among the commonest primary brain tumors and they have a grave prognosis, and so there is an urgent need to develop effective treatment. In this study, we investigated the molecular mechanisms that are responsible for the anti-tumor effect of ginsenosides on human astrocytoma cells. MATERIALS ANDMETHODS:
We tested 13 different ginsenosides for their anti-tumor effect on human malignant astrocytoma cells in conjunction with Fas stimulation. In addition, the cell signaling pathways were explored by using pharmacological inhibitors and performing immunoblot analysis. DCF-DA staining and antioxidant experiments were performed to investigate the role of reactive oxygen species as one of the apoptosis-inducing mechanisms.RESULTS:
Among the 13 different ginsenoside metabolites, compound K and Rh2 induced apoptotic cell death of the astrocytoma cells in a caspase- and p38 MAPK-dependent manner, yet the same treatment had no cytotoxic effect on the primary cultured human astrocytes. Combined treatment with ginsenosides and Fas ligand showed a synergistic cytotoxic effect, which was mediated by the reduction of intracellular reactive oxygen species.CONCLUSION:
These results suggest that ginsenoside metabolites in combination with Fas ligand may provide a new strategy to treat malignant astrocytomas, which are tumors that are quite resistant to conventional anti-cancer treatment.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Prognosis
/
Astrocytoma
/
Brain Neoplasms
/
Astrocytes
/
Cell Death
/
Reactive Oxygen Species
/
Apoptosis
/
Ginsenosides
/
Fas Ligand Protein
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
Cancer Research and Treatment
Year:
2009
Type:
Article
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