Contrasting protective effects of cannabinoids against oxidative stress and amyloid-β evoked neurotoxicity in vitro

Harvey, Benjamin S.; Ohlsson, Katharina S.; Mååg, Jesper L.V.; Musgrave, Ian F.; Smid, Scott D.

doi:10.1016/j.neuro.2011.12.015

Cited by 83Cannabis and Cannabinoid ResearchAlzheimer's disease research and treatmentsParkinson's Disease Mechanisms and Treatments

Contrasting protective effects of cannabinoids against oxidative stress and amyloid-β evoked neurotoxicity in vitro

Harvey, Benjamin S., Ohlsson, Katharina S., Mååg, Jesper L.V., Musgrave, Ian F., Smid, Scott D.·2012·NeuroToxicology

DOI 10.1016/j.neuro.2011.12.015

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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.

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CBD decreases neuronal damage induced by β-amyloid protein deposit.
“CBD decreases the neuronal damage induced by β-amyloid protein deposit (105); (114–116)”
From Translational investigation of the therapeutic potential of Cannabidiol (CBD): Toward a new age (2018) · cites this paper as [116]
CBD exerts antioxidant activities against toxicity induced by different agents, such as amphetamine.
“Furthermore, CBD exerts antioxidant activities against toxicity induced different agents, such as amphetamine (89, 116, 121)”
From Translational investigation of the therapeutic potential of Cannabidiol (CBD): Toward a new age (2018) · cites this paper as [116]
CBD attenuates the depletion of tyrosine hydroxylase, GABA and dopamine levels by modulating the expression of inducible NO synthase and reducing the production of ROS-generating NADPH oxidases.
“and attenuates the depletion of tyrosine hydroxylase, GABA and dopamine levels by modulating the expression of the inducible isoform of NO synthase and reducing the production of ROS-generating NADPH oxidases (114–120).”
From Translational investigation of the therapeutic potential of Cannabidiol (CBD): Toward a new age (2018) · cites this paper as [116]

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Authors: Harvey, B. S., Ohlsson, K. S., Mååg, J. L. V., Musgrave, I. F., & Smid, S. D.
Affiliations: The University of Adelaide (AU)
University of Gothenburg (SE)
Uppsala University (SE)
Corresponding author: Smid, Scott D.
ORCID: Harvey, Benjamin S.
Mååg, Jesper L.V.
Musgrave, Ian F.
Smid, Scott D.
Venue: NeuroToxicology
Publisher: Elsevier BV
Published: 2012-01
Volume: 33
Issue: 1
Pages: 138-146
ISSN: 0161-813X (ISSN-L)
DOI: 10.1016/j.neuro.2011.12.015
OpenAlex: W2069283073
Cited by: 82
References: 55
Citations by year: 2026: 2 · 2025: 3 · 2024: 6 · 2023: 6 · 2022: 4 · 2021: 7 · 2020: 6 · 2019: 5 · 2018: 7 · 2017: 7 · 2016: 3 · 2015: 3 · 2014: 7 · 2013: 11 · 2012: 4
FWCI: 6.11
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: NeuroToxicology (publishedVersion)
PubMed (publishedVersion)
Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
Funders: University of Adelaide
Topics: Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords: cannabinoids, neuroprotection, oxidative stress, amyloid-beta, Alzheimer's disease, anandamide, cannabidiol, CB1 receptor, CB2 receptor, ACEA, JWH-015, hydrogen peroxide, tert-butyl hydroperoxide, PC12 cells, SH-SY5Y cells
MeSH terms: Analysis of Variance, Animals, Antioxidants, Arachidonic Acids, Cannabinoids, Cell Survival, Chromans, Drug Interactions, Gene Expression Regulation, Humans, Hydrogen Peroxide, Indoles, Neuroblastoma, Peptide Fragments, Thiazoles, Lipid Peroxidation, Amyloid beta-Peptides, PC12 Cells, Oxidative Stress, Receptor, Cannabinoid, CB1, Receptor, Cannabinoid, CB2, Cell Line, Tumor, Microscopy, Electron, Transmission, Rats, Benzothiazoles

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Contrasting protective effects of cannabinoids against oxidative stress and amyloid-β evoked neurotoxicity in vitro

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