The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB1)

Grabiec, Urszula; Koch, Marco; Kallendrusch, Sonja; Kraft, Robert A.; Hill, Kerstin; Merkwitz, Claudia; Ghadban, Chalid; Lutz, Beat; Straiker, Alex; Dehghani, Faramarz

doi:10.1016/j.neuropharm.2011.11.023

Cited by 23 publications

(34 citation statements)

References 65 publications

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“…OHSC were prepared from 5 day old C57 Black6/J mice as reported earlier 49 and kept at 35 C in a fully humidified atmosphere with 5% (v/v) CO 2. Culture medium was changed every other day.…”

Section: Organotypic Hippocampal Slice Cultures (Ohsc)mentioning

confidence: 99%

The influence of biomechanical properties and cannabinoids on tumor invasion

Hohmann

Grabiec

Ghadban

et al. 2016

Cell Adhesion & Migration

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Background: Cannabinoids are known to have an anti-tumorous effect, but the underlying mechanisms are only sparsely understood. Mechanical characteristics of tumor cells represent a promising marker to distinguish between tumor cells and the healthy tissue. We tested the hypothesis whether cannabinoids influence the tumor cell specific mechanical and migratory properties and if these factors are a prognostic marker for the invasiveness of tumor cells.Methods: 3 different glioblastoma cell lines were treated with cannabinoids and changes of mechanical and migratory properties of single cells were measured using atomic force microscopy and time lapse imaging. The invasiveness of cell lines was determined using a co-culture model with organotypic hippocampal slice cultures.Results: We found that cannabinoids are capable of influencing migratory and mechanical properties in a cell line specific manner. A network analysis revealed a correlation between a "generalized stiffness" and the invasiveness for all tumor cell lines after 3 and 4 d of invasion time: Conclusions: Here we could show that a "generalized stiffness" is a profound marker for the invasiveness of a tumor cell population in our model and thus might be of high clinical relevance for drug testing. Additionally cannabinoids were shown to be of potential use for therapeutic approaches of glioblastoma.

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Section: Organotypic Hippocampal Slice Cultures (Ohsc)mentioning

confidence: 99%

The influence of biomechanical properties and cannabinoids on tumor invasion

Hohmann

Grabiec

Ghadban

et al. 2016

Cell Adhesion & Migration

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“…An inhibition of oxidative stress may be a potential therapeutic for HIE (Dai et al, 2017; Zhang et al, 2018). It has been shown earlier that NADA exerts antioxidant and neuroprotective activities in different experimental models through mechanisms that are independent of CB1 and TRPV‐1 receptors (Bobrov et al, 2008; Grabiec et al, 2012; Novosadova et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…CB1/TRPV1 receptors were not involved in the effects as well (Novosadova et al, 2017). NADA had a neuroprotective effect in organotypical hippocampal slice cultures after NMDA treatment, partly through CB1 (Grabiec et al, 2012). These data indicate that NADA may act as endogenous antioxidant and neuroprotector in different pathological conditions.…”

Section: Introductionmentioning

confidence: 99%

Early‐life N‐arachidonoyl‐dopamine exposure increases antioxidant capacity of the brain tissues and reduces functional deficits after neonatal hypoxia in rats

Sukhanova

Sebentsova

Khukhareva

et al. 2019

Intl J of Devlp Neuroscience

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Perinatal hypoxia‐ischemia is one of the most common causes of perinatal brain injury and subsequent neurological disorders in children. The aim of this work was to evaluate the potential antioxidant and neuroprotective effects of N‐arachidonoyl‐dopamine (NADA) in the model of acute neonatal hypoxia (ANH) in rat pups. Male and female Wistar rats were exposed to a hypoxic condition (8% oxygen for 120 min) at postnatal day 2 (P2). Transcription factor HIF1‐α and glutathione peroxidases GPx2 and GPx4 gene expression was increased in rat brains in the hypoxic group compared to control 1.5 h but not 4 days after ANH. There were no post‐hypoxic changes in reduced (GSH) and oxidised (GSSG) glutathione levels in the brain of rat pups 1.5 h and 4 d after hypoxia. Hypoxic rats displayed retarded performance in the righting reflex and the negative geotaxis tests. ANH resulted in increased ambulation in Open field test and impaired retention in the Barnes maze task under stressful conditions as compared with the control group. Treatment with NADA significantly attenuated the delayed development of sensorimotor reflexes and stress‐evoked disruption of memory retention in hypoxic rats but had no effect on the hypoxia‐induced hyperactivity. In rats exposed to hypoxia, treatment with NADA decreased GPx2 gene expression and increased GSH/GSSG ratio in whole brains 1.5 h after ANH. These results suggest that the long‐lasting beneficial effects of NADA on hypoxia‐induced neurobehavioural deficits are mediated, at least in part, by its antioxidant properties.

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“…Sections were then washed three times for 10 min with PBS/Triton followed by the incubation with Alexa 488-conjugated goat anti-mouse IgG (1∶200) and Alexa 568- conjugated goat anti-rabbit IgG (1∶500), respectively. Slides were then coversliped with Dako fluorescent mounting medium, and analysed by a Zeiss LSM 510 Meta confocal laser scanning system, as previously described [19], [20]. For ExtrAvidin peroxidase staining, sections were treated with methanol containing 1.5% (v/v) of 30% (v/v) hydrogen peroxide for 10 min.…”

Section: Methodsmentioning

confidence: 99%

Temporal Dynamics of Glyoxalase 1 in Secondary Neuronal Injury

et al. 2014

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BackgroundEnhanced glycolysis leads to elevated levels of the toxic metabolite methylglyoxal which contributes to loss of protein-function, metabolic imbalance and cell death. Neurons were shown being highly susceptible to methylglyoxal toxicity. Glyoxalase 1 as an ubiquitous enzyme reflects the main detoxifying enzyme of methylglyoxal and underlies changes during aging and neurodegeneration. However, little is known about dynamics of Glyoxalase 1 following neuronal lesions so far.MethodsTo determine a possible involvement of Glyoxalase 1 in acute brain injury, we analysed the temporal dynamics of Glyoxalase 1 distribution and expression by immunohistochemistry and Western Blot analysis. Organotypic hippocampal slice cultures were excitotoxically (N-methyl-D-aspartate, 50 µM for 4 hours) lesioned in vitro (5 minutes to 72 hours). Additionally, permanent middle cerebral artery occlusion was performed (75 minutes to 60 days).ResultsWe found (i) a predominant localisation of Glyoxalase 1 in endothelial cells in non-lesioned brains (ii) a time-dependent up-regulation and re-distribution of Glyoxalase 1 in neurons and astrocytes and (iii) a strong increase in Glyoxalase 1 dimers after neuronal injury (24 hours to 72 hours) when compared to monomers of the protein.ConclusionsThe high dynamics of Glyoxalase 1 expression and distribution following neuronal injury may indicate a novel role of Glyoxalase 1.

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The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB1)

Cited by 23 publications

References 65 publications

The influence of biomechanical properties and cannabinoids on tumor invasion

The influence of biomechanical properties and cannabinoids on tumor invasion

Early‐life N‐arachidonoyl‐dopamine exposure increases antioxidant capacity of the brain tissues and reduces functional deficits after neonatal hypoxia in rats

Temporal Dynamics of Glyoxalase 1 in Secondary Neuronal Injury

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