In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid.
Agnese GugliandoloFederica PollastroGianpaolo GrassiPlacido BramantiEmanuela MazzonPublished in: International journal of molecular sciences (2018)
Inflammation and oxidative stress play main roles in neurodegeneration. Interestingly, different natural compounds may be able to exert neuroprotective actions against inflammation and oxidative stress, protecting from neuronal cell loss. Among these natural sources, Cannabis sativa represents a reservoir of compounds exerting beneficial properties, including cannabigerol (CBG), whose antioxidant properties have already been demonstrated in macrophages. Here, we aimed to evaluate the ability of CBG to protect NSC-34 motor neurons against the toxicity induced from the medium of LPS-stimulated RAW 264.7 macrophages. Using MTT assay, we observed that CBG pre-treatment was able to reduce the loss of cell viability induced by the medium of LPS-stimulated macrophages in NSC-34 cells. Indeed, CBG pre-treatment inhibited apoptosis, as shown by the reduction of caspase 3 activation and Bax expression, while Bcl-2 levels increased. Furthermore, CBG pre-treatment counteracted not only inflammation, as demonstrated by the reduction of IL-1β, TNF-α, IFN-γ and PPARγ protein levels assessed by immunocytochemistry, but also oxidative stress in NSC-34 cells treated with the medium of LPS-stimulated RAW 264.7. Indeed, immunocytochemistry showed that CBG pre-treatment reduced nitrotyrosine, SOD1 and iNOS protein levels and restored Nrf-2 levels. All together, these results indicated the neuroprotective effects of CBG, that may be a potential treatment against neuroinflammation and oxidative stress.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- ischemia reperfusion injury
- inflammatory response
- cell death
- cell cycle arrest
- endothelial cells
- immune response
- poor prognosis
- bone marrow
- anti inflammatory
- insulin resistance
- lipopolysaccharide induced
- combination therapy
- climate change
- signaling pathway
- rheumatoid arthritis
- small molecule
- dendritic cells
- blood brain barrier
- brain injury
- risk assessment
- replacement therapy
- cell therapy
- newly diagnosed