[The cannabinoid system and its importance in the perinatal period].

“The cannabinoid system has been recently described, including the endogenous ligands, mainly arachidonic acid derivatives, and their specific receptors. Endocannabinoids are involved in the modulation of synaptic transmission, through which they exert their psychoactive, motor and antinociceptive effects, among others; they also exert extraneural effects, mainly immunomodulation and vasodilation.

Recent data suggest that the cannabinoid system might play an important role in human ontogeny and could participate in the implantation and early development of the embryo, in fetal brain development, and in the beginning of breast feeding after birth.

In addition, the vasodilatory effect of cannabinoids, together with inhibition of the release of excitotoxic amino acids and cytokines, as well as modulation of oxidative stress and the toxic production of nitric oxide, justify the growing evidence pointing to a possible neuroprotective effect of cannabinoids in perinatal asphyxia.”

http://www.ncbi.nlm.nih.gov/pubmed/16266619

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/

Delta-9 tetrahydrocannabinol (THC) inhibits lytic replication of gamma oncogenic herpesviruses in vitro

Figure 2

“The major psychoactive cannabinoid compound of marijuana, delta-9 tetrahydrocannabinol (THC), has been shown to modulate immune responses and lymphocyte function. After primary infection the viral DNA genome of gamma herpesviruses persists in lymphoid cell nuclei in a latent episomal circular form. In response to extracellular signals, the latent virus can be activated, which leads to production of infectious virus progeny. Therefore, we evaluated the potential effects of THC on gamma herpesvirus replication.

THC specifically targets viral and/or cellular mechanisms required for replication and possibly shared by these gamma herpesviruses, and the endocannabinoid system is possibly involved in regulating gamma herpesvirus latency and lytic replication. The immediate early gene ORF 50 promoter activity was specifically inhibited by THC. These studies may also provide the foundation for the development of antiviral strategies utilizing non-psychoactive derivatives of THC.

 We believe that studies on cannabinoids and herpesviruses are important to continue because there are obvious potential benefits. Better understanding may lead to the development of specific non-psychoactive drugs that may inhibit reactivation of oncogenic herpesviruses.”

Cannabis May Help Combat Herpes Viruses

“The compound in marijuana that produces a high, delta-9 tetrahydrocannbinol or THC, may block the spread of several forms of cancer causing herpes viruses, University of South Florida College of Medicine scientists report.

Once a person is infected with herpes, the viruses can remain dormant for long periods within white blood cells before they burst out and begin replicating. This reactivation of the virus boosts the number of cells infected thereby increasing the chances that the cells will become cancerous.

The USF team found that this sudden reactivation was prevented if infected cells were grown in the presence of THC. Furthermore, the researchers showed that THC acts specifically on gamma herpes viruses. The chemical had no effect on another related virus, herpes simplex-1, which causes cold sores and genital herpes.

Small concentrations of THC were found to be more potent and selective against gamma herpes viruses than the commonly used antiviral drugs on the market.

The findings, published Sept. 15 in the online journal BMC Medicine, could lead to the creation of antiviral drugs based on nonpsychoactive derivatives of THC.”

http://stdlabtest.com/2009/06/30/cannabis-may-help-combat-herpes-viruses/

The Cannabinoid WIN55212-2 Promotes Neural Repair After Neonatal Hypoxia–Ischemia

Figure 1.

“In the last years, cannabinoids have emerged as promising neuroprotective agents in several animal paradigms of acute and degenerative brain damage. Most neuroprotective effects of cannabinoids result from the activation of cannabinoid Type 1 (CB1R) and Type 2 (CB2R) receptors in neural and immune cells.

Besides, the stimulating effect of cannabinoids on proliferation, survival, and differentiation of neural progenitor cells provides interesting prospects for long-term neural repair after acute brain damage.

The endocannabinoid system has been involved in the modulation of neural stem cells proliferation, survival and differentiation as well as in the generation of new oligodendrocyte progenitors in the postnatal brain. The present work aims to test the effect of the synthetic Type 1 and Type 2 cannabinoid receptor agonist WIN55212-2 on these processes in the context of neonatal rat brain hypoxia–ischemia (HI)…

Our results suggest that the activation of the endocannabinoid system promotes white and gray matter recovery after neonatal HI injury…

In conclusion, we have demonstrated that the synthetic cannabinoid WIN55212-2 enhances SVZ cell proliferation, oligodendrogenesis, white matter remyelination, and neuroblast generation after neonatal HI.

These findings, summed to the previously described neuroprotective properties of cannabinoids after acute brain damage, may possess therapeutic repercussions in the long-term management of neonatal HI encephalopathy, a prevalent and devastating condition for which no pharmacological treatments are yet available.”

http://stroke.ahajournals.org/content/41/12/2956.full

 

Activation of cannabinoid 2 receptors protects against cerebral ischemia by inhibiting neutrophil recruitment

Figure 1.

“THE CONSEQUENCES OF ISCHEMIC INJURY in liver, heart, and brain can be ameliorated by cannabinoids, a group of diverse compounds that include constituents of the plant Cannabis sativa (phytocannabinoids), endogenous lipids (endocannabinoids), and synthetic substances. Most of the effects of cannabinoids are mediated by the G-protein-coupled receptors cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2)… 

Cannabinoids protect against ischemic stroke…

Activation of the cannabinoid 2 receptor (CB2) reduces ischemic injury in several organs…

In conclusion, our data demonstrate that by activating p38 in neutrophils, CB2 agonists inhibit neutrophil recruitment to the brain and protect against ischemic brain injury.”

http://www.fasebj.org/content/24/3/788.long

Researchers Meet to Discuss Cannabinoid-Based Stroke Therapy

Murikinati et al., 2010 shows that brain tissue is saved after a stroke with JWH-133

“The Cannabinoid Discussion Group at Temple University met for the second time this semester to review a recent scientific publication from a German Laboratory. The presenter was Zachary Reichenbach, an MD/Ph.D student at Temple, who is currently working in the laboratory of Dr.Ron Tuma. The Tuma lab is focused on studying cannabinoid based therapies for the treatment of cerebral ischemia resulting from stroke. Mr.Reichenbach led the discussion on a research paper which showed that the cannabinoid JWH-133 activates the cannabinoid type 2 receptor (CB2R), resulting a decrease in infarct size or brain damage duringreperfusion following an ischemic event.

Mr.Reichenbach provided background on stroke, stating that it is the 3rd cause of death in this country, and 85% of those strokes are of the ischemic variety. During an ischemic event there is a hyper-immune response resulting in the recruitment of immune cells that kill brain tissue. Cannabinoids have been shown to modulate the immune system, notably the Tuma lab has published data on the CB2 receptor’s anti-inflammatory effects. Activating the CB2 receptor decreases the migration of hyper-immune cells to the brain. The more brain you save, the more you save someone from disabilities or death.

When asked about the implications of these findings on a cannabinoid that could be a potential stroke therapy, Mr.Reichenbach replied that the results of his work and others is promising…

And just in case you were wondering, THC, the active ingredient in Cannabis, activates both the CB1 and CB2 receptor.”

http://www.examiner.com/article/researchers-meet-to-discuss-cannabinoid-based-stroke-therapy

Cannabis gives stroke patients hope

“New research by University of Otago scientists suggests some mechanisms in the brain targeted by cannabis could become drugs targets to counter brain cell damage after a stroke.

Researchers from the Medical School’s Department of Pharmacology and Toxicology have been the first in the world to show the cannabinoid CB2 receptor appears in the rat brain following a stroke. Their findings were published recently in the journal Neuroscience Letters.

Dr John Ashton says the CB2 receptor is a protein produced as part of the body’s immune response system.

“This response is triggered by stroke and causes the inflammation that leads to damage in the area of the brain around where the stroke has occurred.

“If the inflammation can be stopped or reduced then it offers the hope of reducing the extent of the damage caused by stroke – and CB2 offers a potential target for such a drug.””

http://www.sciencealert.com.au/news/20071404-15007.html

“Cerebral hypoxia-ischemia and middle cerebral artery occlusion induce expression of the cannabinoid CB2 receptor in the brain. The presence of CB2-positive cells in the brain following stroke may provide a novel strategy for cannabinoid-mediated intervention into stroke induced neurodegeneration without the psychoactive effects of CB1 receptor stimulation.” https://www.ncbi.nlm.nih.gov/pubmed/17123706

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/