“CB2 R stimulation has immunomodulatory effects. This study investigated the effects of CB2 R modulation on leukocyte-endothelial adhesion and inflammatory mediator release in experimental endotoxin-induced uveitis (EIU).
Stimulation of CB2 R is anti-inflammatory in a model of acute EIU by a mechanism involving a reduction in NF-κβ, AP-1 and inflammatory mediators.
CB2 R may be a promising drug target for the development of novel ocular anti-inflammatory agents.”
“Recently, the presence of the endocannabinoid system in hematopoietic and neural stem cells has been demonstrated…
In the present study, we have investigated, through a multidisciplinary approach, the involvement of the endocannabinoids in migration, viability and cytokine release of human mesenchymal stromal cells.
We show, for the first time, that cultures of human mesenchymal stromal cells express all of the components of the endocannabinoid system, suggesting a potential role for the cannabinoid CB2 receptor as a mediator of anti-inflammatory properties of human mesenchymal stromal cells, as well as of their survival pathways and their capability to home and migrate towards endocannabinoid sources.”
“Osteoarthritis (OA) of the joint is a prevalent disease accompanied by chronic, debilitating pain. Recent clinical evidence has demonstrated that central sensitization contributes to OA pain. An improved understanding of how OA joint pathology impacts upon the central processing of pain is crucial for the identification of novel analgesic targets/new therapeutic strategies.
Inhibitory cannabinoid 2 (CB2) receptors attenuate peripheral immune cell function and modulate central neuro-immune responses in models of neurodegeneration…
These findings suggest that targeting CB2 receptors may have therapeutic potential for treating OA pain.”
“This Commenatry highlights the article by Rom et al which shows that selective cannabinoid receptor 2 activation in leukocytes decreases key steps in monocyte-blood brain barrier engagement suppressing inflammatory leukocyte responses and preventing neuroinflammation.”
“Cannabinoid receptor 2 (CB2) is highly expressed in immune cells and stimulation decreases inflammatory responses. We tested the idea that selective CB2 activation in human monocytes suppresses their ability to engage the brain endothelium and migrate across the blood-brain barrier (BBB), preventing consequent injury…
These results indicate that selective CB2 activation in leukocytes decreases key steps in monocyte-BBB engagement, thus suppressing inflammatory leukocyte responses and preventing neuroinflammation.”
“Delta9-tetrahydrocannabinol and other cannabinoids exert pro-apoptotic actions in tumor cells via the CB2 cannabinoid receptor…
Here we used the human leukemia cell line Jurkat-that expresses CB2 as the unique CB receptor-to investigate…
In summary, results presented here show that CB2 receptor activation signals apoptosis via a ceramide-dependent stimulation of the mitochondrial intrinsic pathway.”
“In the current study, we examined whether ligation of CB2 receptors would lead to induction of apoptosis in tumors of immune origin and whether CB2 agonist could be used to treat such cancers.
Exposure of murine tumors EL-4, LSA, and P815 to delta-9-tetrahydrocannabinol (THC) in vitro led to a significant reduction in cell viability and an increase in apoptosis…
Culture of primary acute lymphoblastic leukemia cells with THC in vitro reduced cell viability and induced apoptosis.
Together, the current data demonstrate that CB2 cannabinoid receptors expressed on malignancies of the immune system may serve as potential targets for the induction of apoptosis. Also, because CB2 agonists lack psychotropic effects, they may serve as novel anticancer agents to selectively target and kill tumors of immune origin.”
http://bloodjournal.hematologylibrary.org/content/100/2/627.long
“We examined whether treatment of tumor-bearing mice with THC was effective at killing tumor cells in vivo… These data suggest that THC was effective in vivo to induce apoptosis and kill the tumor cells… THC treatment can cure tumor-bearing mice… they were completely cured…Taken together, these results suggest that THC can exert anticancer properties in vivo.” http://bloodjournal.hematologylibrary.org/content/100/2/627.long?sso-checked=1
“Dr. Lu has been working to find new types of chemotherapeutic drugs that both kill pancreatic cancer and suppress the cancer pain at the same time by targeting a special G-protein coupled receptor that belongs to the biological system responsible for the effects of Tetrahydrocannabinol (THC), a compound derived from some varieties of cannabis (hemp) or made synthetically, that is the primary psychoactive agent in marijuana and hashish.
Dr. Lu says pancreatic cancer cells have more type 2 cannabinoid receptors than do healthy cells.
Consequently, drug molecules that selectively activate this receptor can induce cancer cell death without affecting normal pancreatic cells, noting that when given to mice with pancreatic tumors, the molecule prevented tumor growth and suppressed the spread of cancer to healthy organs.
Meanwhile, this class of compounds also generates painkillers comparable to morphine’s pain killing effect…”
“Navigation of retinal projections towards their targets is regulated by guidance molecules and growth cone transduction mechanisms. Here, we present in vitro and in vivo evidences that the cannabinoid receptor 2 (CB2R) is expressed along the retino-thalamic pathway and exerts a modulatory action on axon guidance….
Overall, this study demonstrates that the contribution of endocannabinoids to brain development is not solely mediated by CB1R, but also involves CB2R.”
“The role of spinal cannabinoid systems in neuropathic pain of streptozotocin-induced diabetic mice was studied…
… A low dose of WIN-55,212-2 significantly recovered the tail-flick latency in streptozotocin-induced diabetic mice… The selective cannabinoid CB2 receptor agonist L-759,656 also dose-dependently recovered the tail-flick latency in streptozotocin-induced diabetic mice…
These results indicate that spinal cannabinoid systems are changed in diabetic mice and suggest that cannabinoid CB2 receptor agonists might have an ability to recover diabetic neuropathic pain.”