Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/76191
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Type: Journal article
Title: Contrasting protective effects of cannabinoids against oxidative stress and amyloid-β evoked neurotoxicity in vitro
Other Titles: Contrasting protective effects of cannabinoids against oxidative stress and amyloid-beta evoked neurotoxicity in vitro
Author: Harvey, B.
Ohlsson, K.
Maag, J.
Musgrave, I.
Smid, S.
Citation: NeuroToxicology, 2012; 33(1):138-146
Publisher: Intox Press Inc
Issue Date: 2012
ISSN: 0161-813X
1872-9711
Statement of
Responsibility: 
Benjamin S. Harvey, Katharina S. Ohlsson, Jesper L.V. Mååg, Ian F. Musgrave, Scott D. Smid
Abstract: Cannabinoids have been widely reported to have neuroprotective properties in vitro and in vivo. In this study we compared the effects of CB1 and CB2 receptor-selective ligands, the endocannabinoid anandamide and the phytocannabinoid cannabidiol, against oxidative stress and the toxic hallmark Alzheimer's protein, β-amyloid (Aβ) in neuronal cell lines. PC12 or SH-SY5Y cells were selectively exposed to either hydrogen peroxide, tert-butyl hydroperoxide or Aβ, alone or in the presence of the CB1 specific agonist arachidonyl-2'-chloroethylamide (ACEA), CB2 specific agonist JWH-015, anandamide or cannabidiol. Cannabidiol improved cell viability in response to tert-butyl hydroperoxide in PC12 and SH-SY5Y cells, while hydrogen peroxide-mediated toxicity was unaffected by cannabidiol pretreatment. Aβ exposure evoked a loss of cell viability in PC12 cells. Of the cannabinoids tested, only anandamide was able to inhibit Aβ-evoked neurotoxicity. ACEA had no effect on Aβ-evoked neurotoxicity, suggesting a CB1 receptor-independent effect of anandamide. JWH-015 pretreatment was also without protective influence on PC12 cells from either pro-oxidant or Aβ exposure. None of the cannabinoids directly inhibited or disrupted preformed Aβ fibrils and aggregates. In conclusion, the endocannabinoid anandamide protects neuronal cells from Aβ exposure via a pathway unrelated to CB1 or CB2 receptor activation. The protective effect of cannabidiol against oxidative stress does not confer protection against Aβ exposure, suggesting divergent pathways for neuroprotection of these two cannabinoids.
Keywords: β-Amyloid
cannabinoid
neuroprotection
oxidative stress
Rights: © 2011 Elsevier Inc. All rights reserved.
DOI: 10.1016/j.neuro.2011.12.015
Published version: http://dx.doi.org/10.1016/j.neuro.2011.12.015
Appears in Collections:Aurora harvest
Pharmacology publications

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