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Cannabidiol, a non‐psychoactive marijuana component, exhibits antioxidant and neuroprotective effects in neuronal Alzheimer's cell model SH‐5Y
Author(s) -
Briggs Gwyneth Helen
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.552.6
Subject(s) - cannabidiol , neuroprotection , chemistry , pharmacology , oxidative stress , antioxidant , lipid peroxide , superoxide dismutase , glutathione , biochemistry , biology , medicine , enzyme , psychiatry , cannabis
Cannabidiol, a non‐psychoactive marijuana component, is a pleotropic PPAR‐gamma agonist which exhibits antioxidant and neuroprotective effects in several experimental models. Amyloid beta (Aβ), the precursor to extracellular senile plaques, has been implicated in the development of cognitive impairment and neuronal cell death. The effect of Cannabidiol against AD pathology has been linked to its ability to attenuate Aβ and tau aggregation in vitro. The present study evaluates the neuroprotective action of Cannabidiol on Aβ‐induced oxidative stress and memory loss. Differentiated SH‐SY5Y neuronal cell lines were pretreated with cannabidiol followed by Aβ treatment for 24 hours. SHSY5Y cells treated with Aβ exhibited increased reactive oxygen species and lipid peroxide levels. Enzymatic antioxidants including superoxide dismutase, catalase and glutathione reductase were decreased in the Aβ treated group when compared to the control group. Aβ treatment also increased the expression of total tau as well as phosphorylated forms of tau (CP13, S202/205; PHF1, S396/404). Expression of PSD‐95 and Arc proteins, essential for synaptic maturity and plasticity, was decreased by Aβ treatment. Cannabidiol treatment attenuated the accumulation of lipid peroxide levels, up‐regulated the antioxidant activities and improved the expression of memory‐associated proteins in Aβ treated SHSY5Y cells. Mechanistic study using SH‐SY5Y cell line transfected with APP695 (SH‐SY5Y‐APP) to investigate the Aβ ameliorating effects of cannabidiol showed no changes in protein levels of APP, α‐secretase or gamma secretase activity. In contrast, cannabidiol decreased β‐secretase levels and inhibited its activity thereby leading to reduced Aβ levels. These results suggest that Cannabidiol is capable of improving antioxidant activity, mitochondrial energy regulation, while decreasing Aβ, thereby indicating it to be a lead compound for AD drug development. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .