CBG activates α2-adrenoceptors and CB2 and blocks CB1 and 5-HT1A receptors (Cascio, Gauson, Stevenson, Ross, & Pertwee, 2010).
Also, CBG activates TRPA1, TRPV1 and TRPV2, antagonizes TRPM8 and inhibits ACU. Botanical drug substance (BDS) containing CBD also inhibits MAGL and NAAA. These receptor interactions suggest that CBG could have analgesic, anti-inflammatory and anti-cancer properties (De Petrocellis et al., 2008, 2011).
CBG modulates GPR55 (Morales, Hurst, & Reggio, 2017)
CBG has antifungal and antibacterial properties (Eisohly, Turner, Clark, & Eisohly, 1982).
CBG counteracts oxidative stress through CB2 receptors (Giacoppo et al., 2017).
CBG inhibits platelet aggregation, which increases bleeding time and reduces thromboembolism (Formukong, Evans, & Evans, 1989).
CBG causes hyperphagia in animals without producing negative neuromotor side effects (Brierley, Samuels, Duncan, Whalley, & Williams, 2016). Also, CBG-BDS acts as an appetite stimulant, probably through CB1 receptors (Brierley, Samuels, Duncan, Whalley, & Williams, 2017).
CBG inhibits cellular growth in human oral epitheloid carcicoma cells (Baek et al., 1998) and showed chemopreventive, curative and pro-apoptotic effects against colorectal cancer cells in vitro and in vivo models through TRPM8 and CB2 receptors (Borrelli et al., 2014).
CBG and related cannabinoids may have therapeutic potential for the treatment of glaucoma.(Colasanti, 1990). Chronic administration of CBG causes ocular hypotensive effects without any toxic effects (Colasanti, Craig, & Allara, 1984). Also, its analog CBG-DMH reduces intraocular pressure (Szczesniak, Maor, Robertson, Hung, & Kelly, 2011).
CBG reduces acetylcholine-induced contractions in the bladder, suggesting a potential effect to treat bladder disorders (Pagano et al., 2015).
CBG can activate α2 receptors and block CB1 and 5-HT1A receptors (Cascio et al., 2010), suggesting CBG does have therapeutic potential in the treatment of depression.
Functional Gastro-Intestinal Disorders
Apart from THC, (relatively) non-psychotropic cannabinoids such as THCV, CBD and CBG were found to have anti-inflammatory effects in experimental intestinal inflammation (Alhouayek and Muccioli, 2012). CBG attenuates colitis in animal models, reduces nitric oxide production in macrophages and reduces ROS formation in intestinal epithelial cells, showing therapeutic potential to treat gastrointestinal inflammation (Borrelli et al., 2013).
CBG counteracts the anti-nausea effects produced by THC or CBD, probably due to the activation of 5-HT1A receptor (Rock et al., 2011). This is important to avoid CBG when looking for anti-nausea and anti-vomiting effects of cannabinoids.
CBG improved motor deficits and had neuroprotective effects in animal models of Huntington´s Disease through the modulation of pro-inflammatory markers, reactive microgliosis and improved antioxidant defenses. CBG also normalized gene expression altered in those animal models (Valdeolivas et al., 2015).
The interaction between CBG and the α2 receptor (alpha 2 adrenalin receptor) may prove effective in pain control (Giovannoni et al., 2009).
CBG could be used to treat psoriasis (Wilkinson & Williamson, 2007) and it shows potential to treat dry-skin syndrome by increasing sebaceous lipid synthesis (Oláh et al., 2016).
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