Renal (kidney) Cancer cells Die When Cannabinoid Receptor Activated

“Add kidney cancer (RCC) to the growing list of individual cancers where the ECS is actively expressed in an attempt to decrease cancer growth. In RCC, specifically CB2R and not CB1R activation cause the cancer cell to die.”

-    Dr. David Hepburn

Abstract:

The anti-tumor properties of cannabinoids have been investigated in many in vitro and in vivo studies. Many of these anti-tumor effects are mediated via cannabinoid receptor types 1 and 2 (CB1 and CB2), comprising the endocannabinoid system (ECS).

In thisstudy, the ECS isinvestigatedbasedon CB1 and CB2 receptor gene and protein expression in renal cell carcinoma (RCC) cell lines. In view of their further use for potential treatments, then the roles of CB1 and CB2 receptorswereinvestigatedin the anti-proliferative action and signal transduction triggered by synthetic cannabinoid agonists [such as JWH-133 and WIN 55,212–2 (WIN-55)] in RCC cell lines.

Read the full article here:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5966919/

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Dr. Dave Hepburn website: https://doctordavidhepburn.com

The New Weed on the Block

“This cannabinomimetic of medical interest in that it might harness the same cannabis receptors without causing some of the unwanted side effects of THC. If it works well, the US government might have to make it illegal.”

- Dr. David Hepburn

Abstract:

The recent discovery of another source of a cannabinoid comes from a plant that is a relative of the mosses called liverwort. One genus of the plant, Radula, boasts a handful of species that produce a chemical that is a lot like tetrahydrocannabinol (THC) from Cannabis sativa, or marijuana.

Why a liverwort, which lives and reproduces quite differently from a plant like Cannabis, would make this molecule remains a mystery. What we now know, however, is the cannabinoid from liverwort and the one in Cannabis are almost exactly the same and have quite similar effects in the mammalian brain.

Read the full article here:

https://www.scientificamerican.com/article/lowly-moss-like-plant-seems-to-copy-cannabis/

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Dr. David Hepburn website: https://doctordavidhepburn.com

Less Morphine Required When Cannabinoid Receptor Activated

“Many pain patients, with time, require increases of dose and/or frequency of the potentially deadly opiate morphine in order to obtain pain control. However, by activation of the CB2 receptor, tolerance and dependance of morphine was diminished.”

- Dr. David Hepburn

Abstract:

Morphine is widely used as an analgesic to treat moderate to severe pain, but chronic morphine use is associated with development of tolerance and dependence, which limits its analgesic efficacy.

A previous research has showed that non analgetic dose of a cannabinoid type 2 (CB2) receptor agonist reduced morphine tolerance in cancer pain. A previous study also showed the colocalization of CB2 and transient receptor potential vanilloid 1 (TRPV1) in human and rat dorsal root ganglia (DRG) sensory neurons.

Read the full article here:

https://www.ncbi.nlm.nih.gov/pubmed/28901432

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Dr. Dave Hepburn website: https://doctordavidhepburn.com

Why Women Don’t Forget

“Men appear to have 41% more CB1 receptors in the brain. Unfortunately for men of the male species, this is inversely related to working memory. (No memory of working). The sex difference in the ECS is becoming more interesting in explaining reactions and abilities in both.”

-    Dr. David Hepburn 

Abstract:

The endocannabinoid system (ECS) has a widespread neuron modulatory function in the central nervous system and is involved in important aspects of brain function including brain development, cortical rhythms, plasticity, reward, and stress sensitivity. 

Many of these effects are mediated via the cannabinoid CB1 receptor (CB1R) subtype. 

Animal studies convincingly have shown the interaction between the ECS and sex hormones, as well as a sex difference of higher brain CB1R in males. Human in vivo studies of sex difference has yielded discrete pant findings.

Read the full article here:

https://www.ncbi.nlm.nih.gov/pubmed/30296558

Dr. David Hepburn website: https://doctordavidhepburn.com

No Change in Hippocampus Volume With Youth Cannabis Users

“A number of studies have found evidence of structural brain changes in teens and young adults who smoke marijuana, however is research indicates that there are no changes into adulthood in the hippocampus (memory).”

-    Dr. David Hepburn 

Abstract:

Cannabis exposure, particularly heavy cannabis use, has been associated with neuroanatomical alterations in regions rich with cannabinoid receptors such as the hippocampus in some but not in other (mainly cross-sectional) studies. However, it remains unclear whether continued heavy cannabis use alters hippocampal volume, and whether an earlier age of onset and/or a higher dosage exacerbate these changes.

Read full article here:

https://www.ncbi.nlm.nih.gov/pubmed/28741422

Dr. David Hepburn website: https://doctordavidhepburn.com

Endocannabinoids Worsen Heart Function After Heart Attack

“The ECS reacts to try to balance our inner milieu when that milieu is disturbed. Sometimes, as our body tries to help itself, it can end up doing some damage. Endocannabinoids do not cause heart attacks, of course, but they are releases in response to this major stressor.”

-   Dr. David Hepburn.

Intravenous administration of endocannabinoid 2-arachidonoylglycerol into wildtype C57BL6 mice induced a rapid increase of blood neutrophil and monocyte counts as measured by flow cytometry.

This effect was blunted when using cannabinoid receptor 2 knockout mice. In response to myocardial infarction induced in wildtype mice, the lipidomic analysis revealed significantly elevated plasma and cardiac levels of the endocannabinoid 2-arachidonoylglycerol 24 h after infarction, but no changes in anandamide, palmitoylethanolamide and oleoylethanolamide.

Read full article here:

https://www.ncbi.nlm.nih.gov/pubmed/30295758

Dr. Dave Hepburn website: https://doctordavidhepburn.com

New Study of Cannabinoids in Prostate Cancer - Dr. David Hepburn

Article recommend by Dr. David Hepburn:

Cannabinoid WIN 55,212-2 induces cell cycle arrest and apoptosis, and inhibits proliferation, migration, invasion, and tumor growth in prostate cancer in a cannabinoid-receptor 2 dependent manner.

Abstract

BACKGROUND: 

Cannabinoids have demonstrated anticarcinogenic properties in a variety of malignancies, including in prostate cancer. In the present study, we explored the anti-cancer effects of the synthetic cannabinoid WIN 55,212-2 (WIN) in prostate cancer. 

METHODS: 

Established prostate cancer cells (PC3, DU145, LNCaP) were treated with varying concentrations of WIN. Cell proliferation was determined by the MTS assay. The anti-migration and anti-invasive potential of WIN was examined by the wound healing assay and the matrigel invasion assay. Cell cycle analysis was performed by flow cytometry, and mechanistic studies were performed by Western blot. Athymic mice (n = 10) were inoculated with human PC3 cells. Once tumors reached 100 mm3 , animals were randomized into two groups: saline control and WIN (5 mg/kg), delivered by intraperitoneal injection three times per week for 3 weeks. 

RESULTS: 

WIN significantly reduced prostate cancer cell proliferation, migration, invasion, induced apoptosis, and arrested cells in Go/G1 phase in a dose-dependent manner. Mechanistic studies revealed these effects were mediated through a pathway involving cell cycle regulators p27, Cdk4, and pRb. Pre-treatment with a CB2 antagonist, AM630, followed by treatment with WIN resulted in a reversal of the anti-proliferation and cell cycle arrest previously seen with WIN alone. In vivo, administration of WIN resulted in a reduction in the tumor growth rate compared to control (P < 0.05). 

CONCLUSIONS: 

The following study provides evidence supporting the use of WIN as a novel therapeutic for prostate cancer.

“Important news for men with prostates and the women who love them (the men...not the prostates). Potential novel therapeutics for this very common cancer that is the second leading cause of cancer death in American men, behind lung cancer.”

Dr. David Hepburn

To read the full article please visit: 

https://www.ncbi.nlm.nih.gov/pubmed/30242861

Dr. David Hepburn website: 

doctordavidhepburn.com

Cannabinoid Receptor (CB1) Plays Crucial Role in Alzheimers Disease - Dr. Dave Hepburn

Article recommend by Dr. Dave Hepburn:

Genetic deletion of CB1 cannabinoid receptors exacerbates the Alzheimer-like symptoms in a transgenic animal model.

Abstract

Activating CB1 cannabinoid receptor has been demonstrated to produce certain therapeutic effects in animal models of Alzheimer's disease (AD). In this study, we evaluated the specific contribution of CB1 receptor to the progression of AD-like pathology in double transgenic APP/PS1 mice. A new mouse strain was generated by crossing APP/PS1 transgenic mice with CB1 knockout mice. Genetic deletion of CB1 drastically reduced the survival of APP/PS1 mice. In spite that CB1 mutant mice bearing the APP/PS1 transgene developed normally, they suddenly died within the first two months of life likely due to spontaneous seizures. This increased mortality could be related to an imbalance in the excitatory/inhibitory transmission in the hippocampus as suggested by the reduced density of inhibitory parvalbumin positive neurons observed in APP/PS1 mice lacking CB1 receptor at 7 weeks of age. We also evaluated the AD-like phenotype of APP/PS1 mice heterozygous for the CB1 deletion at 3 and 6 months of age. The memory impairment associated to APP/PS1 transgene was accelerated in these mice. Neither the soluble levels of Aβ or the density of Aβ plaques were modified in APP/PS1 mice heterozygous for CB1 deletion at any age. However, the reduction in CB1 receptor expression decreased the levels of PSD-95 protein in APP/PS1 mice, suggesting a synaptic dysfunction in these animals that could account for the acceleration of the memory impairment observed. In summary, our results suggest a crucial role for CB1 receptor in the progression of AD-related pathological events.

“Although several studies have shown that type-2 cannabinoid receptor (CB2R) is involved in Alzheimer's disease (AD) pathology, now a crucial role of CB1R has become evident. One of the more exciting areas of cannabis and endocannaboid research.”

Dr. Dave Hepburn

To read the full article please visit: 

https://www.ncbi.nlm.nih.gov/pubmed/30096288

Dr. David Hepburn website: 

doctordavidhepburn.com