Cannabidiol exerts sebostatic and antiinflammatory effects on human sebocytes

CBD prevents excessive lipogenesis induced by “pro-acne agents&#x...

“Acne vulgaris is the most common human skin disease, affecting quality of life of millions worldwide…

Investigation of the cutaneous cannabinoid system seems to be a promising choice when searching for novel therapeutic possibilities…

“Collectively, our findings suggest that, due to the combined lipostatic, antiproliferative, and antiinflammatory effects, CBD has potential as a promising therapeutic agent for the treatment of acne vulgaris…

These data, together with our current findings, point to a promising, cost-effective, and, likely, well-tolerated new strategy for treating acne vulgaris, the most common human skin disease…

…given the extensively documented accumulation of phytocannabinoids from smoked marijuana in the pilosebaceous unit (where they become incorporated into the hair shaft), it is very likely that CBD can reach the sebaceous glands as well, can accumulate, and may well reach “therapeutically sufficient” concentrations there.

Moreover, it is very important to note that, besides the systemic application, one should keep in mind the possibility of the topical administration.”

 http://www.jci.org/articles/view/64628

“Schematic overview of the cellular “anti-acne trinity” of CBD and its proposed mechanism of action.”

Schematic overview of the cellular “anti-acne trinity” of ...

 

The non-psychotropic plant cannabinoids, cannabidivarin (CBDV) and cannabidiol (CBD), activate and desensitize transient receptor potential vanilloid 1 (TRPV1) channels in vitro: potential for the treatment of neuronal hyperexcitability.

“Epilepsy is the most common neurological disorder, with over 50 million people worldwide affected. Recent evidence suggests that the transient receptor potential cation channel subfamily V member 1 (TRPV1) may contribute to the onset and progression of some forms of epilepsy.

Since the two non-psychotropic cannabinoids cannabidivarin (CBDV) and cannabidiol (CBD) exert anticonvulsant activity in vivo and produce TRPV1-mediated intracellular calcium elevation in vitro, we evaluated the effects of these two compounds on TRPV1 channel activation and desensitization and in an in vitro model of epileptiform activity.

These data suggest that CBDV anti-epileptiform effects in the Mg2+-free model are not uniquely mediated via activation of TRPV1. However, TRPV1 was strongly phosphorylated (and hence likely sensitized) in Mg2+-free solution-treated hippocampal tissue, and both capsaicin and CBDV caused TRPV1 dephosphorylation, consistent with TRPV1 desensitization. We propose that CBDV effects on TRP channels should be studied further in different in vitro and in vivo models of epilepsy.”

http://www.ncbi.nlm.nih.gov/pubmed/25029033

Long-Term Cannabidiol Treatment Prevents the Development of Social Recognition Memory Deficits in Alzheimer’s Disease Transgenic Mice.

“Impairments in cognitive ability and widespread pathophysiological changes caused by neurotoxicity, neuroinflammation, oxidative damage, and altered cholesterol homeostasis are associated with Alzheimer’s disease (AD).

Cannabidiol (CBD) has been shown to reverse cognitive deficits of AD transgenic mice and to exert neuroprotective, anti-oxidative, and anti-inflammatory properties in vitro and in vivo…

This study is the first to demonstrate CBD’s ability to prevent the development of a social recognition deficit in AD transgenic mice.

Our findings provide the first evidence that CBD may have potential as a preventative treatment for AD with a particular relevance for symptoms of social withdrawal and facial recognition.”

http://www.ncbi.nlm.nih.gov/pubmed/25024347

Marijuana Compound CBD Can Effectively Treat Schizophrenia

Marijuana Plant

“Cannabidiol (CBD) is a known marijuana compound, and might just be better than antipsychotics at treating schizophrenia.

A preliminary trial has shown this form of treatment to have fewer side effects than traditional methods of treatment…

Since CBD comes from the marijuana plant, political issues are likely to compromise its availability. Extracting the compound from the plant is also expensive.

But the biggest issue scientists face is that CBD is a natural compound, and can’t be patented the way new drugs are. Pharmaceutical companies are therefore not likely to develop it.”

http://www.designntrend.com/articles/14675/20140529/marijuana-compound-cbd-effectively-treat-schizophrenia.htm

http://www.thctotalhealthcare.com/category/schizophrenia/

Marijuana & Stroke: Pot Compounds Protect Brain, New Meta-Study Shows

“Cannabinoids, chemicals related to those found in cannabis could be effective in restoring neurological function by shrinking the area of the brain affected by stroke, according to a new study led by Dr. Tim England, Honorary Consultant Stroke Physician at the University of Nottingham and Royal Derby Hospital.

Stroke, a leading cause of adult disability in the UK leaves over half of all survivors dependent on others for life. Over one million people are living with the effects of stroke and it is reported that in the UK alone, over 150,000 people have a stroke every year. Finding new treatments to help survivors recover quickly has never been more important.

The authors examined 94 studies evaluating the effects of cannabinoids on 1022 mice, monkeys, and male rats. Cannabinoids can be classified into endocannabinoids that occur naturally in the body, phytocannabinoids that are obtained from plant extracts, and synthetic cannabinoids.

A meta-analysis of experimental studies conducted by the researchers at the University of Nottingham identifies the potential of all three categories of these compounds potential to reduce brain damage caused by stroke and help improve brain function after an attack.

The U.S. government sought a patent in 2001 for the naturally occuring marijuana molecule, cannabidiol, for use as a brain protector during stroke. ”

http://blog.sfgate.com/smellthetruth/2013/12/11/marijuana-stroke-pot-compounds-protect-brain-new-meta-study-shows/

Chemicals in Marijuana May Help Stroke Victims

NewsBriefs

“Scientists at the National Institute of Mental Health (NIMH) said a chemical in marijuana may protect the brain from damage inflicted by a stroke.

Their study was reported in the Proceedings of the National Academy of Sciences (Aidan Hampson, et al., “Cannabidiol and Delta-9-tetrahydrocannabinol Are Neuroprotective Antioxidants,” Proceedings of the National Academy of Sciences, July 7, 1998, Vol. 95, Issue 14, p. 8268; “Pot Chemicals Might Inhibit Breast Tumors, Stroke Damage,” Dallas Morning News, July 13, 1998; Vanessa Thorpe, “Chemicals Help Brain Damage After Stroke,” The Independent (UK), July 19, 1998).

NIMH scientists researched the effects of two cannabinoids, cannabidiol and THC, on the brains of rats. THC is the ingredient in marijuana that causes a psychoactive effect. However, cannabidiol is “a better candidate,” in part, because it does not cause a “high” in the patient, said Aidan Hampson, a neuropharmacologist at NIMH who led the study.

The cannabinoids block a neurochemical, known as glutamate, that leads to the formation of toxic oxidizing molecules that kill brain cells. Glutamate is produced in the brain if the oxygen supply is cut off, for example, as the result of blood clot leading to a stroke.

Researchers found that cannabidiol is a more effective antioxidant than vitamins A and E, which already are known to block the damaging effects of glutamate.”

http://www.ndsn.org/julaug98/medmj1.html

The Inhibitory Effects of Cannabidiol on Systemic Malignant Tumors

“Cannabidiol may attenuate tumor growth in a number of other systemic malignancies.

Decreased tumor growth in pulmonary malignancies is seen after administration of cannabidiol.

Tumor metastasis also is markedly attenuated.

Similar attenuation of tumor growth is seen in breast malignancies.

The above examples clearly illustrate the significant antineoplastic effects of cannabidiol.

Hopefully, the next few years will see increased studies to fully and further evaluate these antineoplastic effects.”

https://www.ncbi.nlm.nih.gov/pubmed/23544909

http://www.jpsmjournal.com/article/S0885-3924(13)00115-2/fulltext#article-outline

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

COX-2 and PPAR-γ confer cannabidiol-induced apoptosis of human lung cancer cells.

Figure 7.

“Within the last decade, evidence has been accumulated to suggest an antitumorigenic action of cannabinoids elicited via induction of apoptosis and alternative anticarcinogenic mechanisms… cannabidiol has been shown to elicit pronounced proapoptotic or autophagic effects on different types of tumor cells

This study investigates the role of COX-2 and PPAR-γ in cannabidiol’s proapoptotic and tumor-regressive action. In lung cancer cell lines (A549, H460) and primary cells from a patient with lung cancer, cannabidiol elicited decreased viability associated with apoptosis… our data show a novel proapoptotic mechanism of cannabidiol involving initial upregulation of COX-2 and PPAR-γ…

Collectively, our data strengthen the notion that activation of PPAR-γ may present a promising target for lung cancer therapy.

In addition and to the best of our knowledge, this is the first report to provide an inhibitor-proven tumor-regressive mechanism of cannabidiolin vivo as well as a proapoptotic mechanism confirmed by use of primary lung tumor cells.

Against this background and considering recent findings supporting a profound antimetastatic action of cannabidiol, this cannabinoid may represent a promising anticancer drug.”

http://mct.aacrjournals.org/content/12/1/69.long

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

Targeting multiple cannabinoid antitumor pathways with a resorcinol derivative leads to inhibition of advanced stages of breast cancer.

“The psychoactive cannabinoid Δ9 -tetrahydrocannabinol (THC) and the non-psychoactive cannabinoid cannabidiol(CBD) can both reduce cancer progression each through distinct antitumor pathways.

Our goal was to discover a compound that could efficiently target both cannabinoid antitumor pathways.

KEY RESULTS:

CBD reduced breast cancer metastasis in advanced stages of the disease as the direct result of down-regulating the transcriptional regulator Id1. However, this was associated with moderate increases in survival. We therefore screened for analogs that could co-target cannabinoid antitumor pathways (CBD- and THC-associated) and discovered the compound O-1663. This analog inhibited Id1, produced a marked stimulation of ROS, upregulated autophagy, and induced apoptosis. Of all compounds tested, it was the most potent at inhibiting breast cancer cell proliferation and invasion in culture and metastasis in vivo.

CONCLUSIONS AND IMPLICATIONS:

O-1663 prolonged survival in advanced stages of breast cancer metastasis. Developing compounds that can simultaneously target multiple cannabinoid antitumor pathways efficiently may provide a novel approach for the treatment of patients with metastatic breast cancer.”

http://www.ncbi.nlm.nih.gov/pubmed/24910342

“Anti-cancer effects of resorcinol derivatives on ascitic and solid forms of Ehrlich carcinoma in mice.” http://www.ncbi.nlm.nih.gov/pubmed/13774935

“Ardisiphenol D, a resorcinol derivative identified from Ardisia brevicaulis, exerts antitumor effect through inducing apoptosis in human non-small-cell lung cancer A549 cells.” http://www.ncbi.nlm.nih.gov/pubmed/24392814

“Antitumor effect of resorcinol derivatives from the roots of Ardisia brevicaulis by inducing apoptosis.” http://www.ncbi.nlm.nih.gov/pubmed/21751842

“Resorcinol derivatives from Ardisia maculosa.”  http://www.ncbi.nlm.nih.gov/pubmed/17885843

“Cannabidiol (CBD) is among the major secondary metabolites of Cannabis devoid of the delta-9-tetra-hydrocannabinol psychoactive effects. It is a resorcinol-based compound with a broad spectrum of potential therapeutic properties, including neuroprotective effects in numerous pathological conditions.” https://www.ncbi.nlm.nih.gov/pubmed/28412918

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

Role of Myeloid-Derived Suppressor Cells in Amelioration of Experimental Autoimmune Hepatitis Following Activation of TRPV1 Receptors by Cannabidiol

Figure 1

“Myeloid-derived suppressor cells (MDSCs) are getting increased attention as one of the main regulatory cells of the immune system. They are induced at sites of inflammation and can potently suppress T cell functions. In the current study, we demonstrate how activation of TRPV1 vanilloid receptors can trigger MDSCs, which in turn, can inhibit inflammation and hepatitis…

This study demonstrates for the first time that MDSCs play a critical role in attenuating acute inflammation in the liver, and that agents such as CBD, which trigger MDSCs through activation of TRPV1 vanilloid receptors may constitute a novel therapeutic modality to treat inflammatory diseases.

Cannabidiol (CBD) is a major non-psychoactive cannabinoid component of marijuana.

Together, these studies not only demonstrate that CBD can protect the host from acute liver injury but also provide evidence for the first time that MDSCs may play a critical role in protecting the liver from acute inflammation.

Non-psychoactive cannabinoids such as CBD possess great therapeutic potential in treating various inflammatory liver diseases, including autoimmune hepatitis.”

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3069975/