Cargando…

In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid

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 res...

Descripción completa

Detalles Bibliográficos
Autores principales: Gugliandolo, Agnese, Pollastro, Federica, Grassi, Gianpaolo, Bramanti, Placido, Mazzon, Emanuela
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073490/
https://www.ncbi.nlm.nih.gov/pubmed/29986533
http://dx.doi.org/10.3390/ijms19071992
_version_ 1783344202362388480
author Gugliandolo, Agnese
Pollastro, Federica
Grassi, Gianpaolo
Bramanti, Placido
Mazzon, Emanuela
author_facet Gugliandolo, Agnese
Pollastro, Federica
Grassi, Gianpaolo
Bramanti, Placido
Mazzon, Emanuela
author_sort Gugliandolo, Agnese
collection PubMed
description 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.
format Online
Article
Text
id pubmed-6073490
institution National Center for Biotechnology Information
language English
publishDate 2018
publisher MDPI
record_format MEDLINE/PubMed
spelling pubmed-60734902018-08-13 In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid Gugliandolo, Agnese Pollastro, Federica Grassi, Gianpaolo Bramanti, Placido Mazzon, Emanuela Int J Mol Sci Article 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. MDPI 2018-07-08 /pmc/articles/PMC6073490/ /pubmed/29986533 http://dx.doi.org/10.3390/ijms19071992 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Gugliandolo, Agnese
Pollastro, Federica
Grassi, Gianpaolo
Bramanti, Placido
Mazzon, Emanuela
In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid
title In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid
title_full In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid
title_fullStr In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid
title_full_unstemmed In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid
title_short In Vitro Model of Neuroinflammation: Efficacy of Cannabigerol, a Non-Psychoactive Cannabinoid
title_sort in vitro model of neuroinflammation: efficacy of cannabigerol, a non-psychoactive cannabinoid
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6073490/
https://www.ncbi.nlm.nih.gov/pubmed/29986533
http://dx.doi.org/10.3390/ijms19071992
work_keys_str_mv AT gugliandoloagnese invitromodelofneuroinflammationefficacyofcannabigerolanonpsychoactivecannabinoid
AT pollastrofederica invitromodelofneuroinflammationefficacyofcannabigerolanonpsychoactivecannabinoid
AT grassigianpaolo invitromodelofneuroinflammationefficacyofcannabigerolanonpsychoactivecannabinoid
AT bramantiplacido invitromodelofneuroinflammationefficacyofcannabigerolanonpsychoactivecannabinoid
AT mazzonemanuela invitromodelofneuroinflammationefficacyofcannabigerolanonpsychoactivecannabinoid