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Neuroprotective effect of cannabidiol, a non-psychoactive component from Cannabis sativa , on β-amyloid-induced toxicity in PC12 cells.
- Source :
- Journal of Neurochemistry; 4/1/2004, Vol. 89 Issue 1, p134-141, 8p
- Publication Year :
- 2004
-
Abstract
- Alzheimer's disease is widely held to be associated with oxidative stress due, in part, to the membrane action of β-amyloid peptide aggregates . Here, we studied the effect of cannabidiol, a major non-psychoactive component of the marijuana plant ( Cannabis sativa ) on β-amyloid peptide-induced toxicity in cultured rat pheocromocytoma PC12 cells. Following exposure of cells to β-amyloid peptide (1 µg/mL), a marked reduction in cell survival was observed. This effect was associated with increased reactive oxygen species (ROS) production and lipid peroxidation, as well as caspase 3 (a key enzyme in the apoptosis cell-signalling cascade) appearance, DNA fragmentation and increased intracellular calcium. Treatment of the cells with cannabidiol (10<superscript>−7</superscript> −10<superscript>−4</superscript> m ) prior to β-amyloid peptide exposure significantly elevated cell survival while it decreased ROS production, lipid peroxidation, caspase 3 levels, DNA fragmentation and intracellular calcium. Our results indicate that cannabidiol exerts a combination of neuroprotective, anti-oxidative and anti-apoptotic effects against β-amyloid peptide toxicity, and that inhibition of caspase 3 appearance from its inactive precursor, pro-caspase 3, by cannabidiol is involved in the signalling pathway for this neuroprotection. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00223042
- Volume :
- 89
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Journal of Neurochemistry
- Publication Type :
- Academic Journal
- Accession number :
- 12564419
- Full Text :
- https://doi.org/10.1111/j.1471-4159.2003.02327.x