Abstract Title:

Caffeic acid phenethyl ester preferentially enhanced radiosensitizing and increased oxidative stress in medulloblastoma cell line.

Abstract Source:

Childs Nerv Syst. 2008 Sep;24(9):987-94. Epub 2008 May 10. PMID: 18470517

Abstract Author(s):

Yi-Yen Lee, Chung-Lan Kao, Ping-Hsing Tsai, Tung-Hu Tsai, Shih-Hwa Chiou, Wei-Fong Wu, Hung-Hai Ku, Tai-Tong Wong

Article Affiliation:

Institute of Clinical Medicine, National Yang-Ming University, and Department of Physical Medicine and Rehabilitation, The Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.

Abstract:

OBJECTIVES: Caffeic acid phenethyl ester (CAPE), an active component of propolis, was recently reported to have radiosensitizing effects on medulloblastoma (MB) cells. However, the mechanisms of radiosensitivity involved in medulloblastoma cells are still unclear. The specific aim of this study was to investigate the role of CAPE-induced oxidative stress to influence of radiosensitivity and anti-proliferative effects in medulloblastoma cells.

MATERIALS AND METHODS: Medulloblastoma (Daoy) cells were treated with CAPE in different concentrations and assessed for cell viability. The following were also evaluated: migratory ability, reduced glutathione (GSH) level, reactive oxygen species (ROS) level, nuclear factor-kappaB (NF-kappaB) activity, and apoptosis in CAPE alone, radiation alone, or radiation combined with CAPE in Daoy cells.

RESULTS: The results indicated that CAPE inhibited the growth of Daoy cells. CAPE treatment in Daoy cells could effectively decrease glutathione reductase and significantly increase glutathione peroxidase. Radiation-activated NF-kappaB was reversed by CAPE pretreatment. Finally, the result of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay showed that CAPE treatment can enhance radiation-induced apoptosis in Daoy cells.

CONCLUSIONS: Our study demonstrated the anti-proliferative and radiosensitizing effects of CAPE on MB cells, which may be achievable through depleting GSH, increased ROS activity, and inhibiting NF-kappaB activity.

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