“scientists reported that THC and other cannabinoids such as CBD (cannabidiol) slows growth and/or causes death of certain types of cancer cells growing in laboratory dishes. Some animal studies suggest certain cannabinoids may slow growth and reduce spread of some forms of cancer”
“In the last several years, development of new CBR ligands has become an intense area in cancer research because of the role of the endocannabinoid system in the regulation of cell proliferation and apoptosis…
The therapeutic potential for synthetic small bivalent ligands holds great promise as new lead compounds in a wide range of disparate diseases.”
“Hypothalamic CB1 Cannabinoid Receptors Regulate Energy Balance in Mice” and “The endocannabinoid system: a new target for the regulation of energy balance and metabolism.”
” It is clear, therefore, that there is sufficient anecdotal clinical data and sound experimental data to encourage proper scientific evaluation of the potential therapeutic benefit of cannabis. Although it undoubtedly possesses the potential for psychic and physical dependency, these are considerably less than the undesirable effects of opioids. The time is now appropriate, therefore, for proper evaluation of this ancient remedy.”
“The therapeutic potential of cannabidiol (CBD), the major nonpsychoactive component of cannabis, was explored in murine collagen-induced arthritis (CIA).
CBD was administered after onset of clinical symptoms, and in both models of arthritis the treatment effectively blocked progression of arthritis. CBD was equally effective when administered i.p. or orally.
Clinical improvement was associated with protection of the joints against severe damage.
Taken together, these data show that CBD, through its combined immunosuppressive and anti-inflammatory actions, has a potent anti-arthritic effect in CIA.”
“In the present study, we report that CBD has a beneficial therapeutic action on established CIA, and we explore its mode of action.” http://www.pnas.org/content/97/17/9561.long
“Because cannabinoid receptor agonists are capable of reducing proliferation and inducing apoptosis (cell death) in diverse cancer cells such as glioma, breast cancer, and melanoma, we evaluated whether CB1 is a potential drug target in rhabdomyosarcoma.
Rhabdomyosarcoma (RMS) is the most common soft-tissue sarcoma in children…
Our study shows that treatment with the cannabinoid receptor agonists HU210 (cloned THC from Hebrew University) and Delta(9)-tetrahydrocannabinol (THC from cannabis) lowers the viability of translocation-positive rhabdomyosarcoma cells through the induction of apoptosis…
These results support the notion that cannabinoid receptor agonists could represent a novel targeted approach for treatment of translocation-positive rhabdomyosarcoma.”
“One of the most intriguing and unexplored actions of cannabinoids is their ability to control cell growth. Thus, cannabinoids have been shown to induce antiproliferative effects through the CB1 receptor… we have recently shown that cannabinoids are able to modulate through the CB1 receptor the activity of the PI3K/protein kinase B pathway, which serves as a pivotal antiapoptotic signal…”
“It has been shown that leukemia and glioma cells are sensitive to cannabidiol (CBD)-induced apoptosis (programmed cell death)….the cellular events and sensitivity to CBD-induced apoptosis between murine thymocytes and EL-4 thymoma cells were compared. Cannabidiol markedly induced apoptosis in a time- and concentration-related manner in both cells… The results demonstrated that both thymocytes and EL-4 thymoma cells were susceptible to CBD-induced apoptosis…”
“Cannabidiol-induced apoptosis in primary lymphocytes is associated with oxidative stress-dependent activation of caspase-8” and “The non-psychoactive cannabidiol triggers caspase activation and oxidative stress in human glioma cells… we have shown that the non-psychoactive cannabinoid compound cannabidiol (CBD) induces apoptosis (cell death) of glioma cells in vitro and tumor regression…”
Endocannabinoids including anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are important lipid mediators for immunosuppressive effects and for appropriate homeostasis via their G-protein-coupled cannabinoid (CB) receptors in mammalian organs and tissues, and may be involved in wound healing in some organs. The physiological roles of endocannabinoids in periodontal healing remain unknown. We observed upregulation of the expression of CB1/CB2 receptors localized on fibroblasts and macrophage-like cells in granulation tissue during wound healing in a wound-healing model in rats, as well as an increase in AEA levels in gingival crevicular fluid after periodontal surgery in human patients with periodontitis. In-vitro, the proliferation of human gingival fibroblasts (HGFs) by AEA was significantly attenuated by AM251 and AM630, which are selective antagonists of CB1 and CB2, respectively. CP55940 (CB1/CB2 agonist) induced phosphorylation of the extracellular-regulated kinases (ERK) 1/2, p38 mitogen-activated protein kinase (p38MAPK), and Akt in HGFs. Wound closure by CP55940 in an in-vitro scratch assay was significantly suppressed by inhibitors of MAP kinase kinase (MEK), p38MAPK, and phosphoinositol 3-kinase (PI3-K). These findings suggest that endocannabinoid system may have an important role in periodontal healing.