RELATED STUDY
Manipulation of the Endocannabinoid System in Colitis: A Comprehensive Review.
Key Findings: CB 1 and 2, endogenous cannabinoids, and atypical cannabinoids are upregulated in inflammation, and their presence and stimulation attenuates murine colitis, while cannabinoid receptor antagonism and cannabinoid receptor deficient models reverse these anti-inflammatory effects. In addition, inhibition of endocannabinoid degradation via monoacylglycerol lipase and fatty acid amide hydrolase blockade can also attenuate colitis development, and is closely linked to cannabinoid receptor expression. CB1 and CB2 receptor agonism is largely anti-inflammatory while CB1 and CB2 receptor antagonism is pro-inflammatory.
Type of Study: Meta-analysis
Study Result: Positive
Study Location(s): United States
Year of Pub: 2017
Cannabinoids Studied: AM-x Synthetic Cannabinoids, JWH-x Synthetic Cannabinoids, HU-x Synthetic Cannabinoids, O-x Synthetic Cannabinoids, SR-x Synthetic Cannabinoids, WIN-x Synthetic Cannabinoids, Anandamide (AEA), Fatty Acid Amide Hydrolase (FAAH), 2-Arachidonoyl Glycerol (2-AG), Monoacylglycerol Lipase (MAGL), Cannabinoid (unspecified), Synthetic Cannabinoid (unspecified), Other Related Compounds
Phytocannabinoid Source: Not Applicable
Terpenes Studied: ß-Caryophyllene
Receptors Studied: CB1, CB2, GPCR 55, TRPV1, PPAR - Alpha, GPCR, TRPs, PPARs
Ligands Studied: Anti-inflammatory cytokines, Pro-inflammatory cytokines, Neurotransmitter (unspecified/other)
