“The protective effects of cannabidiol (CBD) have been widely shown in preclinical models and have translated into medicines for the treatment of multiple sclerosis and epilepsy. However, the direct vascular effects of CBD in humans are unknown.
This study shows, for the first time, that CBD causes vasorelaxation of human mesenteric arteries via activation of CB1 and TRP channels, and is endothelium- and nitric oxide-dependent.”
“Cannabidiol (CBD) has anti-inflammatory effects.
We explored its therapeutic effects on cardiac ischemia-reperfusion injury with an experimental imaging platform…
Compared to controls, CBD treatment improved systolic wall thickening, significantly increased blood flow in the AAR, significantly decreased microvascular obstruction, increased the PDR by 1.7-fold, lowered the AMI-core/AAR ratio, and increased the MSI.
These improvements were associated with reductions in serum cTnI, cardiac leukocyte infiltration, and myocellular apoptosis.
Thus, CBD therapy reduced AMI size and facilitated restoration of LV function.
We demonstrated that this experimental platform has potential theragnostic utility.”
“The active molecules in cannabis kill brain cancer — another study has revealed.”
“Scientists using an extract of whole-plant marijuana rich in pot’s main psychoactive ingredient THC as well as cannabidiol (CBD) showed “dramatic reductions in tumor volumes” of a type of brain cancer.” http://blog.sfgate.com/smellthetruth/2014/11/18/marijuana-kills-brain-cancer-new-study-confirms/
“Marijuana kills brain cancer, new study confirms. The active molecules in cannabis kill brain cancer — another study has revealed.” http://blog.seattlepi.com/marijuana/2014/11/18/marijuana-kills-brain-cancer-new-study-confirms/#13130101=0
“Marijuana Kills Brain Cancer Cells. Researchers have found that the THC in marijuana causes brain cancer cells to die in both mice and humans.” http://www.nbcphiladelphia.com/news/health/Marijuana_Kills_Brain_Cancer_Cells_All__National_.html
“Marijuana Kills Brain Cancer, New Study Confirms” http://cancerguide.byethost8.com/marijuana-kills-brain-cancer-new-study-confirms-sfgate-blog/
“Drug addiction is a chronically relapsing disorder characterized by the compulsive desire to use drugs and a loss of control over consumption.
Cannabidiol (CBD), the second most abundant component of cannabis, is thought to modulate various neuronal circuits involved in drug addiction.
The goal of this systematic review is to summarize the available preclinical and clinical data on the impact of CBD on addictive behaviors.
MEDLINE and PubMed were searched for English and French language articles published before 2015. In all, 14 studies were found, 9 of which were conducted on animals and the remaining 5 on humans.
A limited number of preclinical studies suggest that CBD may have therapeutic properties on opioid, cocaine, and psychostimulant addiction, and some preliminary data suggest that it may be beneficial in cannabis and tobacco addiction in humans.
Further studies are clearly necessary to fully evaluate the potential of CBD as an intervention for addictive disorders.”
http://www.ncbi.nlm.nih.gov/pubmed/26056464
“CBD is an exogenous cannabinoid that acts on several neurotransmission systems involved in addiction. Animal studies have shown the possible effects of CBD on opioid and psychostimulant addiction, while human studies presented some preliminary evidence of a beneficial impact of CBD on cannabis and tobacco dependence. CBD has several therapeutic properties on its own that could indirectly be useful in the treatment of addiction disorders, such as its protective effect on stress vulnerability and neurotoxicity… The dreadful burden of substance-use disorder worldwide, combined with the clear need for new medication in the addiction field, justifies the requirement of further studies to evaluate the potential of CBD as a new intervention for addictive behaviors.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4444130/
“Graft-versus-host-disease (GVHD) is a major obstacle to successful allogeneic hematopoietic cell transplantation (alloHCT).
Cannabidiol (CBD), a non-psychotropic ingredient of Cannabis sativa possesses potent anti-inflammatory and immunosuppressive properties. We hypothesized that CBD may decrease GVHD incidence and severity after alloHCT…
The combination of CBD with standard GVHD prophylaxis is a safe and promising strategy to reduce the incidence of acute GVHD. A randomized double blind controlled study is warranted.”
“Smoked marijuana contains over 100 different cannabinoids, including the psychoactive compound Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD).
THC, CBD, and its acidic precursor, cannabidiolic acid (CBDA), have all been shown to have antiemetic properties in the Suncus murinus.
Here we show that when subthreshold antiemetic doses of CBD or CBDA are combined with a subthreshold antiemetic dose of THC in the S. murinus, both lithium-chloride-induced vomiting and abdominal retching are dramatically suppressed.
These results suggest that combined effects of these compounds may lead to better control of vomiting with fewer side effects.”
“Cocaine is a commonly abused illicit drug that causes significant morbidity and mortality. The most severe and common complications are seizures, ischemic strokes, myocardial infarction, and acute liver injury. Here, we demonstrated that acute cocaine intoxication promoted seizure along with acute liver damage in mice, with intense inflammatory infiltrate.
Considering the protective role of the endocannabinoid system against cell toxicity, we hypothesized that treatment with an anandamide hydrolysis inhibitor, URB597, or with a phytocannabinoid, cannabidiol (CBD), protects against cocaine toxicity.
URB597 (1.0 mg/kg) abolished cocaine-induced seizure, yet it did not protect against acute liver injury.
Using confocal liver intravital microscopy, we observed that CBD reduced acute liver inflammation and damage induced by cocaine and prevented associated seizure.
Additionally, we showed that previous liver damage induced by another hepatotoxic drug (acetaminophen) increased seizure and lethality induced by cocaine intoxication, linking hepatotoxicity to seizure dynamics.
These findings suggest that activation of cannabinoid system may have protective actions on both liver and brain induced by cocaine, minimizing inflammatory injury promoted by cocaine, supporting its further clinical application in the treatment of cocaine abuse.”
“In glaucoma, the increased release of glutamate is the major cause of retinal ganglion cell death. Cannabinoids have been demonstrated to protect neuron cultures from glutamate-induced death.
In this study, we test the hypothesis that glutamate causes apoptosis of retinal neurons via the excessive formation of peroxynitrite, and that the neuroprotective effect of the psychotropic Delta9-tetrahydroxycannabinol (THC) or nonpsychotropic cannabidiol (CBD) is via the attenuation of this formation.
These results suggest the potential use of CBD as a novel topical therapy for the treatment of glaucoma.
“Cannabinoid components of marijuana, such as (−)Δ9-tetrahydrocannabinol (THC), or the synthetic cannabinoid WIN55,212-2, have been shown to prevent glutamate- or NMDA-induced neurotoxicity in isolated neurons or in the brain via activation of the cannabinoid receptor subtype CB1.
…the nonpsychotropic component of marijuana, cannabidiol (CBD), and the synthetic nonpsychotropic cannabinoid, HU-211, as well as THC have been demonstrated as potent antioxidants and/or NMDA receptor antagonists that protect neuron cultures from glutamate-induced death or from oxidative stress.
… we demonstrated that THC and CBD are neuroprotective against NMDA-induced retinal injury and that their protective actions are in part because of an effect in reducing formation of lipid peroxides, nitrite/nitrate, and nitrotyrosine.
In addition to possessing neuroprotective or retinal neuroprotective activity as demonstrated here and elsewhere, cannabinoids such as THC, WIN55,212-2, endogenous cannabinoid 2-arachidonoylglycerol, as well as nonpsychotropic HU-211 have been demonstrated to induce dose-related reductions in intraocular pressure in human and in animal models.
This suggests that cannabinoids may offer a multifaceted therapy for glaucoma.
In conclusion, our results indicate that lipid peroxidation and ONOO− formation play an important role in NMDA-induced retinal neurotoxicity and cell loss in the retina, and that THC and CBD, by reducing the formation of these compounds, are effective neuroprotectants.
The present studies could form the basis for the development of new topical therapies for the treatment of glaucoma.”
“Degenerative retinal diseases are characterized by inflammation and microglial activation.
The nonpsychoactive cannabinoid, cannabidiol (CBD), is an anti-inflammatory in models of diabetes and glaucoma.
We tested the hypothesis that retinal inflammation and microglia activation are initiated and sustained by oxidative stress and p38 mitogen-activated protein kinase (MAPK) activation, and that CBD reduces inflammation by blocking these processes…
Retinal inflammation and degeneration in uveitis are caused by oxidative stress.
CBD exerts anti-inflammatory and neuroprotective effects by a mechanism that involves blocking oxidative stress and activation of p38 MAPK and microglia.”
“Cannabinoids are known to possess therapeutic properties including inhibition of oxidation, NMDA receptor-activation, and inflammation.
The present study evaluates the ability of CBD to reduce oxidative stress, preserve BRB function, and prevent neural cell death in experimental diabetes…
These results demonstrate that CBD treatment reduces neurotoxicity, inflammation, and BRB breakdown in diabetic animals through activities that may involve inhibition of p38 MAP kinase.
The nonpsychotropic CBD is a promising candidate for anti-inflammatory and neuroprotective therapeutics.”