Tag Archives: cannabinoid receptors

Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease

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“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

 

Targeting cannabinoid receptors to treat leukemia: role of cross-talk between extrinsic and intrinsic pathways in Delta9-tetrahydrocannabinol (THC)-induced apoptosis of Jurkat cells.

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“Targeting cannabinoid receptors has recently been shown to trigger apoptosis and offers a novel treatment modality against malignancies of the immune system.

  In this study, we used human Jurkat leukemia cell lines with defects in intrinsic and extrinsic signaling pathways to elucidate the mechanism of apoptosis induced by Delta9-tetrahydrocannabinol (THC)…

Together, these data suggest that the intrinsic pathway plays a more critical role in THC-induced apoptosis while the extrinsic pathway may facilitate apoptosis via cross-talk with the intrinsic pathway.”

http://www.ncbi.nlm.nih.gov/pubmed/15978942

Cannabinoid-receptor expression in human leukocytes.

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“Marijuana and many of its constituent cannabinoids influence the central nervous system (CNS), probably through the cannabinoid receptor, which has recently been cloned in rat and human. While numerous reports have also described effects of cannabinoids on the immune system, the observation of both mRNA and cannabinoid receptor has hitherto been exclusively confined to the brain, a reported detection in the testis being the sole example of its presence at the periphery.

Here we report the expression of the cannabinoid receptor on human immune tissues using a highly sensitive polymerase-chain-reaction-based method for mRNA quantification. We show that, although present in a much lower abundance than in brain, cannabinoid receptor transcripts are found in human spleen, tonsils and peripheral blood leukocytes…

The demonstration of cannabinoid-receptor expression at both mRNA and protein levels on human leukocytes provides a molecular basis for cannabinoid action on these cells.”

http://www.ncbi.nlm.nih.gov/pubmed/8508790

Anticancer activity of anandamide in human cutaneous melanoma cells.

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“Cannabinoids are implicated in the control of cell proliferation, but little is known about the role of the endocannabinoid system in human malignant melanoma. This study was aimed at characterizing the in vitro antitumor activity of anandamide (AEA) in A375 melanoma cells…

 Overall, these findings demonstrate that AEA induces cytotoxicity against human melanoma cells in the micromolar range of concentrations through a complex mechanism, which involve COX-2 and LOX-derived product synthesis and CB1 activation. Lipid raft modulation, probably linked to GPR55 activation, might also have a role.”

http://www.ncbi.nlm.nih.gov/pubmed/24041928

Marijuana’s Active Ingredient Targets Deadly Brain Cancer – WebMD

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“If results of a recent rat study hold true in human trials, marijuana could be the treatment of choice for patients with malignant glioma — an especially aggressive and often fatal form of brain cancer.

 No, rats haven’t started smoking pot. But when researchers injected tumorous animals with cannabinoids — the drug’s active ingredient — about a third of them went into remission, and another third lived significantly longer than untreated rats.

The findings appear in the March issue of the journal Nature Medicine…

According to lead researcher Manuel Guzmán, PhD, his team’s previous studies showed that cannabinoids could stop growth and kill cancer cells but did not harm normal cells. The current work examined the action behind this effect and whether it would also work in living animals…

The researchers first caused tumors in the brains of 18 rats. They then injected the animals over the course of seven days with either a natural or artificial cannabinoid, or a placebo for comparison. Additional groups of healthy, tumor-free rats also received the various treatments…

All of the untreated animals with tumors died between days 12 and 18, but those treated with the cannabinoids lived much longer, and had significantly smaller tumors…

There were no negative side effects at all in the healthy animals receiving treatment.”

More:http://www.webmd.com/cancer/news/20000228/marijuanas-active-ingredient-targets-deadly-brain-cancer

“Anti-tumoral action of cannabinoids: Involvement of sustained ceramide accumulation and extracellular signal-regulated kinase activation” http://www.nature.com/nm/journal/v6/n3/abs/nm0300_313.html

Towards a better Cannabis drug.

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“Opium smoking has been mostly replaced by i.v. injection of morphine and heroin and we see cocaine sniffing rather than chewing of coca leaves. Cannabis use – be it of marijuana, hashish or bhang – differs.

Any cannabis cognoscente will insist that the crude material is ‘much better’ than pure Δ9 – tetrahydrocannabinol (THC), the only major psychoactive constituent of cannabis (Mechoulam et al., 1970).

Indeed, although pure THC is available as a drug (named Dronabinol) it is apparently not used illicitly.

The pharmacological/biochemical basis for this difference is not clear and is presumably due to several factors. A major reason seems to be the pharmacokinetic difference between cannabis smoking and the oral administration of THC.

 On smoking, the cannabis effects are noted almost immediately, while a 1.5 – 2 hour delay is observed on oral administration.

A further factor may be conditioning to the smell, although there are no published data along these lines. A further factor may be the presence of the terpenoid CB2 agonist beta-caryophyllene in cannabis (Gertsch et al., 2008).

CB2 agonists are well known to cause numerous effects (mostly of a protective nature) which may counteract some of the effects of THC (Pacher & Mechoulam, 2011).”

http://www.ncbi.nlm.nih.gov/pubmed/24024867

Cannabinoid receptors give cells the tools they need to defend against HIV infection

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“Researchers have reported that when healthy cells were placed in a sample dish with the human immunodeficiency virus (HIV), along with a dose of cannabinoids, the cells, which normally would rather quickly become infected, simply denied entry to the virus, and responded as if it were not a threat at all…
 

HIV isn’t special – cannabinoids don’t like any viruses

The stimulation of the receptors wasn’t just detrimental to the AIDS virus, it increased the cells abilities to defend itself against any number of viruses and bacteria…”

More: http://www.naturalnews.com/035656_cannabinoids_HIV_marijuana.html

Small animal PET imaging of the type 1 cannabinoid receptor in a rodent model for anorexia nervosa.

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“Several lines of evidence strongly implicate a dysfunctional endocannabinoid system (ECS) in eating disorders…

CONCLUSION:

These data point to a widespread transient disturbance of the endocannabinoid transmission, specifically for CB1 receptors in the ABA model. Our data also suggest (1) gender effects on regional CB1 receptor binding in the hippocampus and (2) add further proof to the validity of the ABA model to mimic aspects of human disease.”

http://www.ncbi.nlm.nih.gov/pubmed/24006151

Islet Cannabinoid Receptors: Cellular Distribution and Biological Function.

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“This study aimed to determine the cellular distribution of islet cannabinoid receptors (CBs) and their involvement in the development of metabolic and hormonal changes in rats fed a fructose-rich diet (F)…

Cannabinoid receptors appeared exclusively in islet α cells…

CONCLUSIONS:

Islet CBs would exert an important modulatory role in metabolic homeostasis…

 Selective islet CB1 blockers could be useful to prevent/treat the alterations induced by the intake of unbalanced/unhealthy diets.”

http://www.ncbi.nlm.nih.gov/pubmed/24005231

Cannabinoid receptors as a target for therapy of ovarian cancer

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“Ovarian cancer represents one of the leading cause of cancer-relateddeaths for women and is the most common gynecologic malignancy.In spite of relative low morbidity, ovarian cancer has a highfatality ratio, with overall 5-year survival of less than 30%.At present, there are inadequate treatment options for the managementof advanced ovarian cancer, and therefore development of novelapproaches for treatment of this disease are needed.

Cannabinoids,the active components of Cannabis sativa linnaeous and their derivatives have received considerable attention in recent yearsdue to their diverse pharmacological activities such as cell growth inhibition and tumor regression. To date, two differentcannabinoid receptors have been characterized and cloned frommammalian tissues: the “central” CB1 receptor and the “peripheral”CB2 receptor…

These results support a new therapeutic approach for the treatmentof ovarian cancer. It is also conceivable that with available cannabinoids as lead compounds, non-habit forming agents that have higher biological effects could be developed.”

http://www.aacrmeetingabstracts.org/cgi/content/abstract/2006/1/1084

http://cancerres.aacrjournals.org/content/66/8_Supplement/1084.1