The neuroprotective actions of CBD in AD was also studied by Iuvone et al. [30] by evaluating 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. β-amyloid peptide induced a strong reduction of cell survival as well as an increased reactive oxygen species (ROS) production, lipid peroxidation, caspase 3 (a key enzyme in the apoptosis cell-signalling cascade) appearance, DNA fragmentation and intracellular calcium was osbserved. Treatment of the cells with cannabidiol, 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. These results indicate that cannabidiol exerts a neuroprotective effects against β-amyloid peptide toxicity suggesting the a possible involvement of cannabidiol in the signalling pathway for this neuroprotection. This hypothesis was supported by a further study where CBD inhibited both nitrite production and nitric oxide synthase (iNOS) protein expression induced by beta-A [31]. These results of in vitro studies were confirmed in vivo with a mouse model of AD-related neuroinflammation. Mice were inoculated with human beta-A into the right dorsal hippocampus, and treated daily with vehicle or CBD (2.5 or 10 mg kg, i.p.) for 7 days. In contrast to vehicle, CBD dose-dependent significantly inhibited mRNA for glial fibrillary acidic protein and the protein expression in beta-A injected animals. Moreover, under the same experimental conditions, CBD impaired iNOS and IL-1beta protein expression, and the related NO and IL-1beta release [32]. The possibility of CBD inhibiting beta-A-induced neurodegeneration is very promising to AD prevention
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