Receptors and molecular properties
CBG can be found in cannabis plants and some analogue forms of CBG can be found in the Helichrysum umbraculigerum plant (Pollastro et al., 2018).
CBG binds to both CB1 and CB2 receptors, having higher affinity for CB2 (Navarro et al., 2018; Rosenthaler et al., 2014).
CBG, as well as CBD, is a NAV channel blocker but did not show anticonvulsant effects (Hill et al., 2014).
CBG activates α2-adrenoceptors and CB2 and blocks CB1 and 5-HT1A receptors (Cascio et al., 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 anologues also actívate TRPA1 (Lopatriello et al., 2018).
CBG modulates GPR55 (Morales et al., 2017).
Δ9-THC, Δ8-THC, CBN, CBD, CBG, and CBC are directly metabolized by CYP2J2 and inhibit human cardiac CYP2J2 (Arnold et al., 2018)
CBG inhibits platelet aggregation, which increases bleeding time and reduces thromboembolism (Formukong et al., 1989).
ALS / Parkinson’s disease / Huntington’s disease / neurodegeneration
In cultured motorneurons, 2.5 and 5 mM CBG, both alone and in combination with CBD could reduce neuroinflammation and apoptosis in a PPARg-dependent manner (Mammana et al., 2019). This suggests CBG may have therapeutic value in the treatment of ALS and other neurodegenerative diseases.
Also in other studies CBG showed anti-inflammatory properties (Petrosino et al., 2018), counteracted oxidative stress through CB2 receptors in macrophages (Giacoppo et al., 2017) and showed neuroprotective and anti-inflammatory effects for NSC-34 motor neurons by reducing caspase 3 activation, Bax expression, IL-1β, TNF-α, IFN-γ, pparγ, nitrotyrosine, SOD1 and iNOS protein levels (Gugliandolo et al., 2018).
In cultured NSC-43 motor neurons, CBG and CBD reduced pro-apoptotic signaling and altered glutamate, GABA and dopamine signaling suggesting neuroprotective effects (Gugliandolo et al., 2020).
The CBG quinone derivative VCE-003.2 has neuroprotective effects against an animal model of amyotrophic lateral sclerosis (Rodríguez-Cueto et al., 2018) and animal and cell models of Parkinsons disease (García et al., 2018, Burgaz et al., 2020). VCE-003 also improved subventricular zone-derived neurogenesis in response to huntingtin-induced neurodegeneration (Aguareles et al., 2019). Moreover, VCE-003 promoted neuronal progenitor cell survival in a pparγ-dependent way and prevented neuronal loss in mouse models of Huntington’s disease, improving motor deficits, suggesting therapeutic potential in Huntington’s disease and other neurodegenerative diseases (Díaz-Alonso et al., 2016).
Anorexia / cachexia
CBG causes hyperphagia in animals without producing negative neuromotor side effects (Brierley et al., 2016). Also, CBG-BDS acts as an appetite stimulant, probably through CB1 receptors (Brierley et al., 2017). CBG also attenuates cisplatin chemotherapy-induced cachexia in rats: 60 or 120 mg/kg CBG increased food intake and reduced weight loss (Brierley et al., 2019).
CBG has antifungal and antibacterial properties (Eisohly et al., 1982).
CBG has antibiotic activity against Streptococcus Mutants and prevents biofilm formation suggesting potential as an antibiotic and in the prevention of dental caries (Aqawi et al., 2021, 2021). Similarly, CBG prevents quorum sensing and biofilm formation of Vibrio Harveyi, a pathogenic bacterium in fish and invertebrates (Aqawi et al., 2020).
In cultured rat astrocytes, CBG (and to a larger extent CBD) had antioxidant effects suggesting a potentially protective role in neurological disorders such as ischemia (di Giacomo et al., 2020).
CBG inhibits cellular growth in human oral epitheloid carcicoma cells (Baek et al., 1998) and in leukaemic cells (Scott, Shah, Dalgleish, & Liu, 2013) 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 would act more effectively agianst leukaemic cells if it would be mixed with CBD (Scott, Dalgleish, & Liu, 2017; Scott et al., 2013). In cultured glioblastoma cells, CBG reduced tumor cell viability to a similar extent as THC. Moreover, CBG in combination with CBD was more effective than CBG in combination with THC suggesting the non-psychoactive combination of CBG and CBD can be used to treat glioblastoma instead of the potentially psychoactive combination of CBD and THC which is currently often used (Lah et al., 2021).
Cystitis / bladder function
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.
CBG/CBGA as well as CBD/CBDA extracts reduced aldose reductase activity in vivo, suggesting a potential effect on Diabetes (Smeriglio et al., 2018).
In culture and in vivo, CBG and other cannabinoids such as CBD, CBDA, CBGA and THCV (all at 5 mM) increased the viability of bone marrow-derived mesenchymal stem cells. The same concentration of CBG and CBD, both alone and in combination, promote maturation of these stem cells into adipocytes. Insulin signaling was also improved, suggesting CBG and/or CBD might restore energy homeostasis in metabolic disorders such a type 2 Diabetes (Fellous et al., 2020).
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 & 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).
In rodent colitis models, CBG strongly reduced myeloperoxidase activity, suggesting anti-inflammatory potential in the gut (Couch et al., 2018).
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 et al., 1984). Also, its analog CBG-DMH reduces intraocular pressure (Szczesniak et al., 2011).
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).
In the Experimental Autoimmune Encephalitis mouse model for Multiple Sclerosis, a synthetic derivative of CBG (VCE-003) reduced disease intensity and neurological defects via CB2 and PPARg receptors. VCE-003 reduced CD4+ T cell infiltration and Th1/Th17 inflammatory signaling, resulting in reduced microglial activation, myelin sheet preservation and reduced axonal damage, suggesting therapeutic potential for CBD in Multiple Sclerosis (Carrillo-Salinas et al., 2014).
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.
The interaction between CBG and the α2 receptor (alpha 2 adrenalin receptor) may prove effective in pain control (Giovannoni et al., 2009).
In rat dorsal root ganglion neurons, CBG, as well as CBD and THC was capable of blocking subsequent capsaicin responses, suggesting desensitization of TRPV1 receptors. CBG reduced the capsaicin response by 88%, THC by 97%, CBD by 99% and a 1:1:1 combination completely blocked the capsaicin response, suggesting analgesic potential (Anand et al., 2021).
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). Also, CBG, as well as CBD, are involved in skin cell proliferation and differenciation, which can have an effect in skin diseases (Pucci et al., 2013)
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