Abstract
(1) Background: Over the past 10 years, a number of scientific studies have demonstrated the therapeutic potential of cannabinoid compounds present in the Cannabis Sativa and Indica plants. However, their role in mechanisms leading to neurodegeneration following cerebral ischemia is yet unclear. (2) Methods: We investigated the effects of Cannabis extracts (Bedrocan, FM2) or selected cannabinoids (Δ9-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabigerol) in rat organotypic hippocampal slices exposed to oxygen-glucose deprivation (OGD), an in vitro model of forebrain global ischemia. Cell death in the CA1 subregion of slices was quantified by propidium iodide fluorescence, and morphological analysis and tissue organization were examined by immunohistochemistry and confocal microscopy. (3) Results: Incubation with the Bedrocan extract or THC exacerbated, whereas incubation with the FM2 extract or cannabidiol attenuated CA1 injury induced by OGD. Δ9-THC toxicity was prevented by CB1 receptor antagonists, the neuroprotective effect of cannabidiol was blocked by TRPV2, 5-HT1A, and PPARγ antagonists. Confocal microscopy confirmed that CBD, but not THC, had a significant protective effect toward neuronal damage and tissue disorganization caused by OGD in organotypic hippocampal slices. (4) Conclusions: Our results suggest that cannabinoids play different roles in the mechanisms of post-ischemic neuronal death. In particular, appropriate concentrations of CBD or CBD/THC ratios may represent a valid therapeutic intervention in the treatment of post-ischemic neuronal death.
Highlights
Cannabis (Cannabis Sativa), known as marijuana, has been used as a medicinal and recreational drug for centuries
(2) Methods: We investigated the effects of Cannabis extracts (Bedrocan, FM2) or selected cannabinoids (∆9-tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabigerol) in rat organotypic hippocampal slices exposed to oxygen-glucose deprivation (OGD), an in vitro model of forebrain global ischemia
(3) Results: Incubation with the Bedrocan extract or THC exacerbated, whereas incubation with the FM2 extract or cannabidiol attenuated CA1 injury induced by OGD. ∆9-THC toxicity was prevented by CB1 receptor antagonists, the neuroprotective effect of cannabidiol was blocked by TRPV2, 5-hydroxytrypamine 1A (5-HT1A), and peroxisome proliferator-activated receptorγ (PPARγ) antagonists
Summary
Cannabis (Cannabis Sativa), known as marijuana, has been used as a medicinal and recreational drug for centuries. THC accounts for most of the psychotropic effects of Cannabis (including perception alterations, rewarding effects, hyperphagia, and abuse potential), while CBD appears to lack these typical “∆9-THC-like” properties [2]. In many countries, including Italy, it is possible to administer Cannabis extracts or drugs for therapeutic purposes under medical prescription for some specific uses, including chronic pain in multiple sclerosis, nausea and vomiting caused by chemotherapy, anorexia, and cachexia in cancer patients or patients suffering from AIDS, and for the reduction in involuntary body and facial movements in the Gilles de la Tourette syndrome [3,4]
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