Neuroprotective and Neuromodulatory Effects Induced by Cannabidiol and Cannabigerol in Rat Hypo-E22 cells and Isolated Hypothalamus.
cannabidiol
cannabigerol
hypothalamus
kinurenine pathway
neuropeptide
neurotransmitter
Journal
Antioxidants (Basel, Switzerland)
ISSN: 2076-3921
Titre abrégé: Antioxidants (Basel)
Pays: Switzerland
ID NLM: 101668981
Informations de publication
Date de publication:
13 Jan 2020
13 Jan 2020
Historique:
received:
09
12
2019
revised:
23
12
2019
accepted:
10
01
2020
entrez:
17
1
2020
pubmed:
17
1
2020
medline:
17
1
2020
Statut:
epublish
Résumé
Cannabidiol (CBD) and cannabigerol (CBG) are non-psychotropic terpenophenols isolated from Rat hypothalamic Hypo-E22 cells and isolated tissues were exposed to either CBD or CBG, and the gene expressions of neuropeptide (NP)Y, pro-opiomelanocortin (POMC) and fatty acid amide hydrolase were assessed. In parallel, the influence of CBD on the synthesis and release of dopamine (DA), norepinephrine (NE), and serotonin (5-HT) was evaluated. The 3-hydroxykinurenine/kinurenic acid (3-HK/KA) ratio was also determined. Both CBD and CBG inhibited NPY and POMC gene expression and decreased the 3-HK/KA ratio in the hypothalamus. The same compounds also reduced hypothalamic NE synthesis and DA release, whereas the sole CBD inhibited 5-HT synthesis. The CBD modulates hypothalamic neuromodulators consistently with its anorexigenic role, whereas the CBG effect on the same mediators suggests alternative mechanisms, possibly involving peripheral pathways.
Sections du résumé
BACKGROUND
BACKGROUND
Cannabidiol (CBD) and cannabigerol (CBG) are non-psychotropic terpenophenols isolated from
METHODS
METHODS
Rat hypothalamic Hypo-E22 cells and isolated tissues were exposed to either CBD or CBG, and the gene expressions of neuropeptide (NP)Y, pro-opiomelanocortin (POMC) and fatty acid amide hydrolase were assessed. In parallel, the influence of CBD on the synthesis and release of dopamine (DA), norepinephrine (NE), and serotonin (5-HT) was evaluated. The 3-hydroxykinurenine/kinurenic acid (3-HK/KA) ratio was also determined.
RESULTS
RESULTS
Both CBD and CBG inhibited NPY and POMC gene expression and decreased the 3-HK/KA ratio in the hypothalamus. The same compounds also reduced hypothalamic NE synthesis and DA release, whereas the sole CBD inhibited 5-HT synthesis.
CONCLUSION
CONCLUSIONS
The CBD modulates hypothalamic neuromodulators consistently with its anorexigenic role, whereas the CBG effect on the same mediators suggests alternative mechanisms, possibly involving peripheral pathways.
Identifiants
pubmed: 31941059
pii: antiox9010071
doi: 10.3390/antiox9010071
pmc: PMC7022242
pii:
doi:
Types de publication
Journal Article
Langues
eng
Références
Br J Pharmacol. 2017 Oct;174(19):3242-3256
pubmed: 28268256
Trends Pharmacol Sci. 2007 Nov;28(11):567-72
pubmed: 18029031
J Neuroinflammation. 2016 May 27;13(1):124
pubmed: 27233247
Nature. 2000 Apr 6;404(6778):661-71
pubmed: 10766253
Addict Biol. 2019 Jun 19;:e12783
pubmed: 31215752
Anal Cell Pathol (Amst). 2018 Sep 20;2018:1270483
pubmed: 30327755
Life Sci. 1993;53(9):669-79
pubmed: 8102768
Eur J Neurosci. 2012 May;35(10):1605-12
pubmed: 22515201
Methods. 2001 Dec;25(4):402-8
pubmed: 11846609
Eur J Pharmacol. 2010 Sep 1;641(2-3):142-7
pubmed: 20553917
Behav Pharmacol. 2017 Jun;28(4):280-284
pubmed: 28125508
J Neuroinflammation. 2018 Jan 04;15(1):3
pubmed: 29301550
Pharmacol Res. 2016 Nov;113(Pt A):376-383
pubmed: 27641926
Front Pharmacol. 2014 Mar 05;5:37
pubmed: 24634659
Nature. 2015 Mar 5;519(7541):45-50
pubmed: 25707796
Pharmacol Rep. 2017 Dec;69(6):1402-1407
pubmed: 29145068
Neurobiol Dis. 2009 May;34(2):300-7
pubmed: 19385063
Br J Pharmacol. 2011 Aug;163(7):1479-94
pubmed: 21175579
J Biol Chem. 2012 Oct 26;287(44):36944-67
pubmed: 22952224
Neurotherapeutics. 2015 Oct;12(4):699-730
pubmed: 26264914
Brain Res. 1993 Nov 19;628(1-2):128-36
pubmed: 8313139
Peptides. 2014 Jan;51:115-21
pubmed: 24269538
Eur J Pharmacol. 2013 Sep 15;716(1-3):41-53
pubmed: 23500197
Peptides. 2013 Jun;44:66-74
pubmed: 23538212
Psychopharmacology (Berl). 2016 Oct;233(19-20):3603-13
pubmed: 27503475
Endocr Rev. 1999 Feb;20(1):68-100
pubmed: 10047974
Br J Pharmacol. 2015 Oct;172(20):4790-805
pubmed: 26218440
Pharmacotherapy. 2016 Jul;36(7):781-96
pubmed: 27285147
Mol Metab. 2017 Jan 27;6(4):374-381
pubmed: 28377876
Br J Pharmacol. 2010 Jan;159(1):129-41
pubmed: 20002104
Molecules. 2018 Nov 24;23(12):
pubmed: 30477219
Eur J Pharmacol. 2004 Jun 16;493(1-3):41-4
pubmed: 15189762
Int J Immunopathol Pharmacol. 2005 Apr-Jun;18(2):201-12
pubmed: 15888244
Nutr Res Rev. 2014 Jun;27(1):172-85
pubmed: 24933167
Cell Mol Life Sci. 2018 Oct;75(20):3663-3681
pubmed: 30027295
J Proteome Res. 2010 Apr 5;9(4):1965-75
pubmed: 20141220
Neurosci Lett. 2011 Feb 18;490(1):82-4
pubmed: 21172406
Brain Behav Immun. 2019 Jul;79:244-255
pubmed: 30790702
Nutr Metab Cardiovasc Dis. 2008 Feb;18(2):158-68
pubmed: 18061414
Peptides. 2008 Aug;29(8):1377-81
pubmed: 18502539
Front Mol Neurosci. 2019 Jan 15;11:487
pubmed: 30697147
Nature. 2001 Apr 12;410(6830):822-5
pubmed: 11298451
J Neurosci. 1995 Oct;15(10):6640-50
pubmed: 7472425
Eur J Pharmacol. 1999 May 21;372(3):237-40
pubmed: 10395017
J Physiol Pharmacol. 2015 Apr;66(2):181-90
pubmed: 25903949
Nat Rev Drug Discov. 2013 Aug;12(8):630-44
pubmed: 23903222