The non-psychoactive cannabidiol triggers caspase activation and oxidative stress in human glioma cells |
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Authors: | P Massi A Vaccani S Bianchessi B Costa P Macchi D Parolaro |
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Institution: | (1) Department of Pharmacology, Chemotherapy and Medical Toxicology, University of Milan, via Vanvitelli 32, 20129 Milan, Italy;(2) Department of Structural and Functional Biology, Pharmacology Section, Center of Neuroscience, University of Insubria, via A. da Giussano 10, 21052 Busto Arsizio, Varese, Italy;(3) Department of Biotechnology and Bioscience, University of Milano-Bicocca, Piazza della Scienza 2, 20126 Milano, Italy;(4) Center for Brain Research, Department of Neuronal Biology, Medical University of Vienna, Spitalgasse 4, Vienna, Austria |
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Abstract: | Recently, we have shown that the non-psychoactive cannabinoid compound cannabidiol (CBD) induces apoptosis of glioma cells
in vitro and tumor regression in vivo. The present study investigated a possible involvement of caspase activation and reactive oxygen species (ROS) induction
in the apoptotic effect of CBD. CBD produced a gradual, time-dependent activation of caspase-3, which preceded the appearance
of apoptotic death. In addiction, release of cytochrome c and caspase-9 and caspase-8 activation were detected. The exposure
to CBD caused in glioma cells an early production of ROS, depletion of intracellular glutathione and increase activity of
glutathione reductase and glutathione peroxidase enzymes. Under the same experimental condition, CBD did not impair primary
glia. Thus, we found a different sensitivity to the anti-proliferative effect of CBD in human glioma cells and non-transformed
cells that appears closely related to a selective ability of CBD in inducing ROS production and caspase activation in tumor
cells.
Received 6 April 2006; received after revision 31 May 2006; accepted 22 June 2006 |
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Keywords: | Cannabidiol glioma cells caspases reactive oxygen species oxidative stress primary glial culture |
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