Abstract
Cannabidiol (CBD) and cannabigerol (CBG) are Cannabis sativa terpenophenols. Although CBD’s effectiveness against neurological diseases has already been demonstrated, nothing is known about CBG. Therefore, a comparison of the effects of these compounds was performed in two experimental models mimicking the oxidative stress and neurotoxicity occurring in neurological diseases. Rat astrocytes were exposed to hydrogen peroxide and cell viability, reactive oxygen species production and apoptosis occurrence were investigated. Cortexes were exposed to K+ 60 mM depolarizing stimulus and serotonin (5-HT) turnover, 3-hydroxykinurenine and kynurenic acid levels were measured. A proteomic analysis and bioinformatics and docking studies were performed. Both compounds exerted antioxidant effects in astrocytes and restored the cortex level of 5-HT depleted by neurotoxic stimuli, whereas sole CBD restored the basal levels of 3-hydroxykinurenine and kynurenic acid. CBG was less effective than CBD in restoring the levels of proteins involved in neurotransmitter exocytosis. Docking analyses predicted the inhibitory effects of these compounds towards the neurokinin B receptor. Conclusion: The results in the in vitro system suggest brain non-neuronal cells as a target in the treatment of oxidative conditions, whereas findings in the ex vivo system and docking analyses imply the potential roles of CBD and CBG as neuroprotective agents.
Highlights
Cannabis sativa belongs to the Cannabaceae family and is classified in the three recognized varieties sativa, indica and ruderalis
A supra-physiological depolarizing stimulus (K+ 60 mM) [22] was administered to the cortexes in order to reproduce the pathophysiological conditions that are common in various neurological diseases, namely migraine, hypoxia/ischemia and epilepsy [23]. Following treatment with both CBD and CBG, the turnover of 5-HT was determined alongside proteomic analysis and bioinformatics and docking studies. These analyses aimed to investigate the possible mechanisms underlying the effects of the two compounds on cell survival and exocytosis processes leading to 5-HT release
The protection exerted by the two compounds on the astrocyte cell line suggests that the treatment of oxidative conditions should take into consideration the targeting of non-neuronal brain cells
Summary
Cannabis sativa belongs to the Cannabaceae family and is classified in the three recognized varieties sativa, indica and ruderalis. It is a medicinal plant characterized by a phytocomplex rich in secondary metabolites (more than 500), with at least 100 terpenophenolic compounds [1]. The activation of the 5-hydroxytryptamine receptor 1A (5-HT1A) is considered as one of the main mechanisms underlying the neuroprotective effects of CBD in neurological diseases [7,8,9]. Cannabigerol (CBG), another C. sativa terpenophenol which shares a similar mechanism of action with CBD, was reported to act as a neuroprotective agent and to bind to the 5-HT1A receptor. The effect of these two compounds on brain 5-HT synthesis and release, in the framework of pro-oxidant/pro-inflammatory conditions underlying neurological disorders, needs to be better elucidated
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