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; Smid, Scott D.

doi:10.1016/j.neuro.2011.12.015

Cited by 73 publications

(50 citation statements)

References 54 publications

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“…Several other studies have confirmed the neuroprotective potential of cannabinoids, resulting in reduced neuronal cell death from a variety of insults, e.g. excitotoxicity (Shen and Thayer, 1998;Sanchez and Garca-Merino, 2012), oxidative stress (Harvey et al, 2012), hypoxia (Sinor et al, 2000), cerebral ischemia/stroke (Nagayama et al, 1999;Landucci et al, 2011) and traumatic brain injury (Panikashvili et al, 2001;Shohami et al, 2011). KN38-7271 effects on eMCAO-dependent infarct size reduction remained significant, if the first drug administration was delayed 4 h post eMCAO.…”

Section: Discussionmentioning

confidence: 83%

Cannabinoid receptor subtypes 1 and 2 mediate long-lasting neuroprotection and improve motor behavior deficits after transient focal cerebral ischemia

Schmidt¹,

Schäfer²,

Striggow³

et al. 2012

Neuroscience

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Section: Discussionmentioning

confidence: 83%

Cannabinoid receptor subtypes 1 and 2 mediate long-lasting neuroprotection and improve motor behavior deficits after transient focal cerebral ischemia

Schmidt¹,

Schäfer²,

Striggow³

et al. 2012

Neuroscience

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“…Several researchers have demonstrated that the potent neuroprotective property of CBD is associated with its antioxidant capacity [6], [7], so we explored the effects of CBD on OGD/R-induced oxidative stress by detecting the relevant biomarkers. Significant increases in MDA and mitochondrial ROS levels (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Increasing evidence indicates that CBD is a molecule with potentially neuroprotective properties that can be used to treat neurodegenerative disorders. CBD had been shown to reverse the reduction in neuronal viability and the increased excitoxicity, inflammation, and oxidative stress in newborn piglets with hypoxic–ischemic brain damage by targeting the receptors of 5HT 1A and CB 2 [5]; and to protect PC12 and SH-SYS5 cells from tert -butyl-hydroperoxide-induced oxidative stress, independently of the CB 1 and CB 2 receptors [6]. CBD also displays better protective activity against glutamate neurotoxicity than either ascorbate or alpha-tocopherol, which suggests that it is a potentially effective antioxidant [7].…”

Section: Introductionmentioning

confidence: 99%

Cannabidiol attenuates OGD/R-induced damage by enhancing mitochondrial bioenergetics and modulating glucose metabolism via pentose-phosphate pathway in hippocampal neurons

Sun

Wu³

et al. 2017

Redox Biology

142

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Deficient bioenergetics and diminished redox conservation have been implicated in the development of cerebral ischemia/reperfusion injury. In this study, the mechanisms underlying the neuroprotective effects of cannabidiol (CBD), a nonpsychotropic compound derived from Cannabis sativa with FDA-approved antiepilepsy properties, were studied in vitro using an oxygen–glucose-deprivation/reperfusion (OGD/R) model in a mouse hippocampal neuronal cell line. CBD supplementation during reperfusion rescued OGD/R-induced cell death, attenuated intracellular ROS generation and lipid peroxidation, and simultaneously reversed the abnormal changes in antioxidant biomarkers. Using the Seahorse XFe24 Extracellular Flux Analyzer, we found that CBD significantly improved basal respiration, ATP-linked oxygen consumption rate, and the spare respiratory capacity, and augmented glucose consumption in OGD/R-injured neurons. The activation of glucose 6-phosphate dehydrogenase and the preservation of the NADPH/NADP+ ratio implies that the pentose-phosphate pathway is stimulated by CBD, thus protecting hippocampal neurons from OGD/R injury. This study is the first to document the neuroprotective effects of CBD against OGD/R insult, which depend in part on attenuating oxidative stress, enhancing mitochondrial bioenergetics, and modulating glucose metabolism via the pentose-phosphate pathway, thus preserving both energy and the redox balance.

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“…Other studies have shown that neuroprotective effects of CBD are associated with its antioxidant properties (Table 2). CBD decreases the neuronal damage promoted by β-amyloid protein deposit (Iuvone et al, 2004; Esposito et al, 2006, 2011; Sagredo et al, 2007; Harvey et al, 2012; Janefjord et al, 2014; Scuderi et al, 2014) and attenuates the depletion of tyrosine hydroxylase, dopamine, and GABA levels by modulating the expression of the inducible isoform of nitric oxide synthase and reducing the production of ROS-generating NADPH oxidases (Esposito et al, 2006, 2007; Garcia-Arencibia et al, 2007; Sagredo et al, 2007, 2011; Pan et al, 2009). These effects seem to occur, in part, by activation of PPARγ receptors (Esposito et al, 2011; Scuderi et al, 2014) and ubiquitination of amyloid precursor protein (Scuderi et al, 2014).…”

Section: Mechanisms Of Cbd Effects In Neuropsychiatric Disordersmentioning

confidence: 99%

Plastic and Neuroprotective Mechanisms Involved in the Therapeutic Effects of Cannabidiol in Psychiatric Disorders

et al. 2017

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Beneficial effects of cannabidiol (CBD) have been described for a wide range of psychiatric disorders, including anxiety, psychosis, and depression. The mechanisms responsible for these effects, however, are still poorly understood. Similar to clinical antidepressant or atypical antipsychotic drugs, recent findings clearly indicate that CBD, either acutely or repeatedly administered, induces plastic changes. For example, CBD attenuates the decrease in hippocampal neurogenesis and dendrite spines density induced by chronic stress and prevents microglia activation and the decrease in the number of parvalbumin-positive GABA neurons in a pharmacological model of schizophrenia. More recently, it was found that CBD modulates cell fate regulatory pathways such as autophagy and others critical pathways for neuronal survival in neurodegenerative experimental models, suggesting the potential benefit of CBD treatment for psychiatric/cognitive symptoms associated with neurodegeneration. These changes and their possible association with CBD beneficial effects in psychiatric disorders are reviewed here.

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

Cited by 73 publications

References 54 publications

Cannabinoid receptor subtypes 1 and 2 mediate long-lasting neuroprotection and improve motor behavior deficits after transient focal cerebral ischemia

Cannabinoid receptor subtypes 1 and 2 mediate long-lasting neuroprotection and improve motor behavior deficits after transient focal cerebral ischemia

Cannabidiol attenuates OGD/R-induced damage by enhancing mitochondrial bioenergetics and modulating glucose metabolism via pentose-phosphate pathway in hippocampal neurons

Plastic and Neuroprotective Mechanisms Involved in the Therapeutic Effects of Cannabidiol in Psychiatric Disorders

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