Document Detail

Effects of cannabinoids and cannabinoid-enriched Cannabis extracts on TRP channels and endocannabinoid metabolic enzymes.
MedLine Citation:
PMID:  21175579     Owner:  NLM     Status:  MEDLINE    
BACKGROUND AND PURPOSE: Cannabidiol (CBD) and Δ(9) -tetrahydrocannabinol (THC) interact with transient receptor potential (TRP) channels and enzymes of the endocannabinoid system.
EXPERIMENTAL APPROACH: The effects of 11 pure cannabinoids and botanical extracts [botanical drug substance (BDS)] from Cannabis varieties selected to contain a more abundant cannabinoid, on TRPV1, TRPV2, TRPM8, TRPA1, human recombinant diacylglycerol lipase α (DAGLα), rat brain fatty acid amide hydrolase (FAAH), COS cell monoacylglycerol lipase (MAGL), human recombinant N-acylethanolamine acid amide hydrolase (NAAA) and anandamide cellular uptake (ACU) by RBL-2H3 cells, were studied using fluorescence-based calcium assays in transfected cells and radiolabelled substrate-based enzymatic assays. Cannabinol (CBN), cannabichromene (CBC), the acids (CBDA, CBGA, THCA) and propyl homologues (CBDV, CBGV, THCV) of CBD, cannabigerol (CBG) and THC, and tetrahydrocannabivarin acid (THCVA) were also tested.
KEY RESULTS: CBD, CBG, CBGV and THCV stimulated and desensitized human TRPV1. CBC, CBD and CBN were potent rat TRPA1 agonists and desensitizers, but THCV-BDS was the most potent compound at this target. CBG-BDS and THCV-BDS were the most potent rat TRPM8 antagonists. All non-acid cannabinoids, except CBC and CBN, potently activated and desensitized rat TRPV2. CBDV and all the acids inhibited DAGLα. Some BDS, but not the pure compounds, inhibited MAGL. CBD was the only compound to inhibit FAAH, whereas the BDS of CBC > CBG > CBGV inhibited NAAA. CBC = CBG > CBD inhibited ACU, as did the BDS of THCVA, CBGV, CBDA and THCA, but the latter extracts were more potent inhibitors.
CONCLUSIONS AND IMPLICATIONS: These results are relevant to the analgesic, anti-inflammatory and anti-cancer effects of cannabinoids and Cannabis extracts.
Luciano De Petrocellis; Alessia Ligresti; Aniello Schiano Moriello; Marco Allarà; Tiziana Bisogno; Stefania Petrosino; Colin G Stott; Vincenzo Di Marzo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  British journal of pharmacology     Volume:  163     ISSN:  1476-5381     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-07-13     Completed Date:  2012-01-18     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1479-94     Citation Subset:  IM    
Copyright Information:
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.
Endocannabinoid Research Group, Institute of Cybernetics, CNR, Pozzuoli (NA), Italy.
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MeSH Terms
Amidohydrolases / metabolism
Arachidonic Acids / metabolism
COS Cells
Cannabinoid Receptor Modulators / metabolism*
Cannabinoids / pharmacology*
Cannabis / chemistry*
Cercopithecus aethiops
Glycerides / metabolism
HEK293 Cells
Lipoprotein Lipase / metabolism
Monoacylglycerol Lipases / metabolism
Palmitic Acids / metabolism
Plant Extracts / pharmacology
Polyunsaturated Alkamides / metabolism
Transient Receptor Potential Channels / agonists*,  antagonists & inhibitors*,  metabolism
Reg. No./Substance:
0/Arachidonic Acids; 0/Cannabinoid Receptor Modulators; 0/Cannabinoids; 0/Endocannabinoids; 0/Ethanolamines; 0/Glycerides; 0/Palmitic Acids; 0/Plant Extracts; 0/Polyunsaturated Alkamides; 0/Transient Receptor Potential Channels; 53847-30-6/2-arachidonylglycerol; 544-31-0/palmidrol; 94421-68-8/anandamide; EC Lipases; EC Lipase; EC lipase alpha, human; EC 3.5.-/Amidohydrolases; EC 3.5.1.-/NAAA protein, human; EC 3.5.1.-/fatty-acid amide hydrolase

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