Author Archives: David Worrell

Cannabinoid receptors in atherosclerosis.

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“…cannabinoid receptors are potential targets for the treatment of atherosclerosis…

Cannabinoids, such as Delta9-tetrahydrocannabinol, the major psychoactive compound of marijuana… was shown to inhibit disease progression through pleiotropic effects on inflammatory cells.

The development of novel cannabinoid receptor ligands that selectively target CB2 receptors or pharmacological modulation of the endocannabinoid system might offer novel therapeutic strategies in the treatment of atherosclerosis.

The immunomodulatory capacity of cannabinoids is now well established and suggests a broad therapeutic potential of cannabinoids for a variety of conditions, including atherosclerosis.”

http://www.ncbi.nlm.nih.gov/pubmed/16960500

http://www.thctotalhealthcare.com/category/atherosclerosis-2/

“Activation of CB(2) receptors with Delta(9)-tetrahydrocannabinol (THC) has been shown to inhibit atherosclerotic plaque progression in mice, mainly by inhibiting macrophage recruitment.”

http://www.ncbi.nlm.nih.gov/pubmed/18426500

Cannabinoid receptors in acute and chronic complications of atherosclerosis

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“Atherosclerosis is a chronic inflammatory disease that is the primary cause of myocardial infarction and stroke, which occur after sudden thrombotic occlusion of an artery.

A growing body of evidence suggests that cannabinoid signalling plays a fundamental role in atherosclerosis development and its clinical manifestations. Thus, CB2 receptors are protective in myocardial ischaemia/reperfusion and implicated in the modulation of chemotaxis, which is crucial for the recruitment of leukocytes during inflammation.

Delta-9-Tetrahydrocannabinol (THC)-mediated activation has been shown to inhibit atherosclerotic plaque progression in a CB2 dependent manner.

It is tempting to suggest that pharmacological modulation of the endocannabinoid system is a potential novel therapeutic strategy in the treatment of atherosclerosis.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219535/

Activation of cannabinoid CB2 receptor ameliorates atherosclerosis associated with suppression of adhesion molecules.

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“Adhesion molecules have been implicated in the development and progression of atherosclerosis. Cannabinoids have been reported to modulate the migration and adhesion molecules expression of various cell types.

Here we examined the effects of WIN55212-2, a cannabinoid receptor 1 (CB1-R)/cannabinoid receptor 2 (CB2-R) agonist on the development of atherosclerotic lesions…

WIN55212-2 seems to have direct anti-atherosclerotic effects in an animal model of atherosclerosis… these beneficial effects of WIN55212-2 may be mediated through the CB2 receptor.”

http://www.ncbi.nlm.nih.gov/pubmed/20075743

“Activation of CB(2) receptors with Delta(9)-tetrahydrocannabinol (THC) has been shown to inhibit atherosclerotic plaque progression in mice, mainly by inhibiting macrophage recruitment.”

http://www.ncbi.nlm.nih.gov/pubmed/18426500

Towards a therapeutic use of selective CB2 cannabinoid receptor ligands for atherosclerosis.

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“Atherosclerosis remains the primary cause of heart disease and stroke, causing approximately 50% of all deaths in Western countries. The identification of promising novel anti-atherosclerotic therapies is therefore of great interest and represents a continued challenge to the medical community.

Cannabinoids, such as Delta9-tetrahydrocannabinol (THC), which is the major psychoactive compound of marijuana, modulate immune functions and might therefore be of therapeutic use for the treatment of inflammatory diseases.

The authors have demonstrated recently that oral treatment with low dose THC inhibits atherosclerosis progression in mice through pleiotropic immunomodulatory effects on inflammatory cells. All these effects were mediated via the cannabinoid receptor CB(2), the main cannabinoid receptor expressed on immune cells.

The identification and characterization of cannabinoid derivative that selectively activate CB(2) receptors and are devoid of adverse effects might offer a novel therapeutic strategy for the treatment of atherosclerosis.”

http://www.ncbi.nlm.nih.gov/pubmed/19804131

https://www.futuremedicine.com/doi/abs/10.2217/14796678.2.1.49

“Researchers suggest that THC and other cannabinoids, which are active at CB2, the cannabinoid receptor expressed on immune cells, may be valuable in treating atherosclerosis.” https://www.medscape.com/viewarticle/787468

Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice

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Figure 1 : The cannabinoid receptor CB2 is expressed in human and mouse atherosclerotic plaques. Unfortunately we are unable to provide accessible alternative text for this. If you require assistance to access this image, or to obtain a text description, please contact npg@nature.com

“Atherosclerosis is a chronic inflammatory disease… Derivatives of cannabinoids such as delta-9-tetrahydrocannabinol (THC) modulate immune functions and therefore have potential for the treatment of inflammatory diseases.

We investigated the effects of THC in a murine model of established atherosclerosis.

Oral administration of THC resulted in significant inhibition of disease progression.

Our data demonstrate that oral treatment with a low dose of THC inhibits atherosclerosis progression in the apolipoprotein E knockout mouse model, through pleiotropic immunomodulatory effects on lymphoid and myeloid cells.

Thus, THC or cannabinoids with activity at the CB2 receptor may be valuable targets for treating atherosclerosis.”

http://www.nature.com/nature/journal/v434/n7034/full/nature03389.html

http://www.ncbi.nlm.nih.gov/pubmed/15815632

 

Marijuana Chemical Fights Hardened Arteries – WebMD

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WebMD: Better information. Better health.

“The active ingredient in marijuana that produces changes in brain messages appears to fight atherosclerosis — a hardening of the arteries.

It takes a very specific amount of THC — marijuana’s key chemical — to help the arteries. That dose is too low to produce mood-altering effects in the brain, according to the new study.

“It would be difficult to achieve such specific concentrations in the blood by smoking marijuana,” Roth explains in a Nature editorial.”

http://www.webmd.com/heart-disease/news/20050406/marijuana-chemical-fights-hardened-arteries

“Low dose oral cannabinoid therapy reduces progression of atherosclerosis in mice” http://www.nature.com/nature/journal/v434/n7034/full/nature03389.html

 http://www.thctotalhealthcare.com/category/atherosclerosis-2/

CBD-Rich Marijuana Fights Colon Cancer, New Study Finds

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“In 2008, over one million individuals were diagnosed with colon cancer, also known as colorectal cancer or bowel cancer and it caused over 600,000 deaths globally. The results of a study published in the journal Phytomedicine in October 2013 suggest that a botanical extract made from high-CBD (cannabidiol) cannabis can selectively target colon cancer cells, while leaving healthy cells unharmed.

Researchers were able to reduce tumor growth and pre-cancerous lesions in mice with colon cancer using the pot molecule CBD as part of a “botanical drug substance”. The authors believe that CBD’s benefits as demonstrated by the results of the study could have clinical relevance for the use of cannabis-based medicines in cancer patients.

Current colon cancer treatments are not only very toxic but also fail to prevent the progression of the disease in some patients. Disease incidence and mortality have not reduced using screening strategies for colon cancer.

Researchers have made progress in investigating cannabis as a treatment for breast and brain cancers considering its antiproliferative CB1 and CB2-mediated effects in colorectal cancer cells and action in experimental models of colon cancer. The study was partially funded through grants from GW Pharmaceuticals and lead by researchers from Italy and the UK.”

http://blog.sfgate.com/smellthetruth/2014/01/06/cbd-rich-marijuana-fights-colon-cancer-new-study-finds/

“Inhibition of colon carcinogenesis by a standardized Cannabis sativa extract with high content of cannabidiol” http://www.ncbi.nlm.nih.gov/pubmed/24373545

http://www.thctotalhealthcare.com/category/colon-cancer/

The Effect of Cannabidiol on Ischemia/Reperfusion-Induced Ventricular Arrhythmias: The Role of Adenosine A1 Receptors.

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“Cannabidiol (CBD) is a nonpsychoactive phytocannabinoid with anti-inflammatory activity mediated by enhancing adenosine signaling.

As the adenosine A1 receptor activation confers protection against ischemia/reperfusion (I/R)-induced ventricular arrhythmias, we hypothesized that CBD may have antiarrhythmic effect through the activation of adenosine A1 receptor.

Cannabidiol has recently been shown to suppress ischemia-induced ventricular arrhythmias…

The present results demonstrated that CBD has an antiarrhythmic effect against I/R-induced arrhythmias, and the antiarrhythmic effect of CBD may be mediated through the activation of adenosine A1 receptor.”

http://www.ncbi.nlm.nih.gov/pubmed/24853683

Δ8-Tetrahydrocannabivarin prevents hepatic ischaemia/reperfusion injury by decreasing oxidative stress and inflammatory responses through cannabinoid CB2 receptors.

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“Activation of cannabinoid CB(2) receptors protects against various forms of ischaemia-reperfusion (I/R) injury.

Δ(8) -Tetrahydrocannabivarin (Δ(8) -THCV) is a synthetic analogue of the plant cannabinoid Δ(9) -tetrahydrocannabivarin, which exhibits anti-inflammatory effects in rodents involving activation of CB(2) receptors. Here, we assessed effects of Δ(8) -THCV and its metabolite 11-OH-Δ(8) -THCV on CB(2) receptors and against hepatic I/R injury.

CONCLUSIONS AND IMPLICATIONS:

Δ(8) -THCV activated CB(2) receptors in vitro, and decreased tissue injury and inflammation in vivo, associated with I/R partly via CB(2) receptor activation.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3423240/

The plant cannabinoid Delta9-tetrahydrocannabivarin can decrease signs of inflammation and inflammatory pain in mice.

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“The phytocannabinoid, Delta(9)-tetrahydrocannabivarin (THCV), can block cannabinoid CB(1) receptors… THCV can activate CB(2) receptors… THCV can activate CB2 receptors and decrease signs of inflammation and inflammatory pain in mice partly via CB1 and/or CB2 receptor activation…

Because there is evidence that THCV can behave as a CB1 receptor antagonist in vivo, it would also be of interest to explore the possibility that this compound can suppress unwanted symptoms in animal models of disorders in which symptoms can be ameliorated by a combination of CB2 receptor activation and CB1 receptor blockade…”  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2931567/