Category Archives: THC (Delta-9-Tetrahydrocannabinol)

Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1.

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“Delta(9)-Tetrahydrocannabinol, the active agent of Cannabis sativa, exhibits well-documented antitumor properties, but little is known about the possible effects mediated by endogenous cannabinoids on human tumors. In the present study, we analyzed the effect of arachidonyl ethanolamide (AEA) on cervical carcinoma (CxCa) cell lines.

The major finding was that AEA induced apoptosis of CxCa cell lines via aberrantly expressed vanilloid receptor-1, whereas AEA binding to the classical CB1 and CB2 cannabinoid receptors mediated a protective effect…

Overall, these data suggest that the specific targeting of VR1 by endogenous cannabinoids or synthetic molecules offers attractive opportunities for the development of novel potent anticancer drugs.”

http://www.ncbi.nlm.nih.gov/pubmed/15047233

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

Differential role of cannabinoids in the pathogenesis of skin cancer.

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“Cannabinoids (CB) like ∆9-tetrahydrocannabinol (THC) can induce cancer cell apoptosis and inhibit angiogenesis.

Here we investigated the role of exogenous and endogenous cannabinoids in mouse skin cancer.

THC significantly inhibited tumor growth of transplanted HCmel12 melanomas in a CB receptor-dependent manner in vivo through antagonistic effects on its characteristic pro-inflammatory microenvironment.

Our results confirm the value of exogenous cannabinoids for the treatment of melanoma…”

http://www.ncbi.nlm.nih.gov/pubmed/25921771

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

Inhaled cannabis reduces pain in diabetic peripheral neuropathy patients, study suggests

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“A small study finds that inhaling cannabis could demonstrate a dose-dependent pain reduction in patients with diabetic peripheral neuropathy.

Researchers at the University of California, United States conducted a study in which 16 patients with painful diabetic peripheral neuropathy were given placebo, or single doses of cannabis.

These doses were either low (one per cent tetrahydrocannibinol, THC), medium (four per cent THC) or high (seven per cent THC).

Tests were first performed on baseline spontaneous pain, evoked pain and cognitive function. Subsequently, participants either inhaled the cannabis or placebo, with measurements of pain intensity and cognitive function assessed over a three-hour period.

The higher the content of THC participants inhaled, the less pain they felt. The high dose of THC had a significant effect when researchers evoked pain using foam brush and von Frey.

These are tools used to test neuropathic pain in patients – von Frey are a set of filaments that test the pain of a patients by pushing against the skin to assess when the sensation becomes painful.

Patients on the high dose of THC showed impaired performance on the neuropsychological tests, but researchers concluded the pain reduction of patients adds further evidence on the efficacy of cannabis in treating diabetic peripheral neuropathy.

The results of this study were published in the Journal of Pain and Palliative Care Pharmacology.

Earlier this month, the CBD compound in cannabis was reported by researchers as a potential treatment for diabetes.”

http://www.diabetes.co.uk/news/2015/apr/inhaled-cannabis-reduces-pain-in-diabetic-peripheral-neuropathy-patients,-study-suggests-95680845.html

“Efficacy of Inhaled Cannabis on Painful Diabetic Neuropathy.”  http://www.ncbi.nlm.nih.gov/pubmed/25843054

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

The Antitumor Activity of Plant-Derived Non-Psychoactive Cannabinoids.

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“As a therapeutic agent, most people are familiar with the palliative effects of the primary psychoactive constituent of Cannabis sativa (CS), Δ9-tetrahydrocannabinol (THC), a molecule active at both the cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptor subtypes.

Through the activation primarily of CB1 receptors in the central nervous system, THC can reduce nausea, emesis and pain in cancer patients undergoing chemotherapy.

During the last decade, however, several studies have now shown that CB1 and CB2 receptor agonists can act as direct antitumor agents in a variety of aggressive cancers.

In addition to THC, there are many other cannabinoids found in CS, and a majority produces little to no psychoactivity due to the inability to activate cannabinoid receptors.

For example, the second most abundant cannabinoid in CS is the non-psychoactive cannabidiol (CBD). Using animal models, CBD has been shown to inhibit the progression of many types of cancer including glioblastoma (GBM), breast, lung, prostate and colon cancer.

This review will center on mechanisms by which CBD, and other plant-derived cannabinoids inefficient at activating cannabinoid receptors, inhibit tumor cell viability, invasion, metastasis, angiogenesis, and the stem-like potential of cancer cells.

We will also discuss the ability of non-psychoactive cannabinoids to induce autophagy and apoptotic-mediated cancer cell death, and enhance the activity of first-line agents commonly used in cancer treatment.”

Alkylindole-sensitive receptors modulate microglial cell migration and proliferation.

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“Ligands targeting G protein-coupled receptors (GPCR) expressed by microglia have been shown to regulate distinct components of their activation process, including cell proliferation, migration and differentiation into M1 or M2 phenotypes.

Cannabinoids, including the active component of the Cannabis plant, tetrahydrocannabinol (THC), and the synthetic alkylindole (AI) compound, WIN55212-2 (WIN-2), activate two molecularly identified GPCRs: CB1 and CB2 .

Our results suggest that microglia express functional AI-sensitive receptors that control select components of their activation process.

Agonists of these novel targets might represent a novel class of therapeutics to influence the microglial cell activation process. ”

http://www.ncbi.nlm.nih.gov/pubmed/25914169

Cannabis has been shown to kill cancer cells

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“The use of Cannabis for medicinal purposes dates back to ancient times.” http://www.cancer.gov/cancertopics/pdq/cam/cannabis/patient/page1

“Cannabis has been used for medicinal purposes for thousands of years.” http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page1

“The use of Cannabis for medicinal purposes dates back at least 3,000 years. It came into use in Western medicine in the 19th century and was said to relieve pain, inflammation, spasms, and convulsions.” http://www.cancer.gov/cancertopics/pdq/cam/cannabis/patient/page2

“Cannabis has been shown to kill cancer cells in the laboratory”  http://www.cancer.gov/cancertopics/pdq/cam/cannabis/patient/page1

“…cannabinoids may be able to kill cancer cells while protecting normal cells…

A laboratory study of delta-9-THC… showed that it damaged or killed the cancer cells…

A laboratory study of cannabidiol… showed that it caused cancer cell death…” http://www.cancer.gov/cancertopics/pdq/cam/cannabis/patient/page2

“Cannabinoids appear to kill tumor cells but do not effect their nontransformed counterparts and may even protect them from cell death.” http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page4

“Because cannabinoid receptors, unlike opioid receptors, are not located in the brainstem areas controlling respiration, lethal overdoses from Cannabis and cannabinoids do not occur.” http://www.cancer.gov/cancertopics/pdq/cam/cannabis/healthprofessional/page6

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

[The role of endocannabinoid system in physiological and pathological processes in the eye].

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“Plant of Cannabis sativa/ marihuana except for its psychotropic effects possesses a range of pharmacological properties, that has been utilized for medical purposes over a period of millenia.

Investigations concerning biochemical mechanism of action of the main and most active pharmacological compound of Cannabis sativa, cannabinoid 9-THC, contributed to the discovery of cannabinoid receptors both in the central nervous system (CNS) and peripheral tissues, that mediated actions of this substance.

The discovery made possible identification of a new, endogenous signaling system referred to as the endocannabinoid system.

Besides cannabinoid receptors CB1 and CB2, the system includes it’s endogenic ligands (endocannabinoids) and compounds that participate in their biosynthesis and inactivation. Structure and functioning of the endocannabinoid system is conservative in all vertebrates.

It’s activation with plant, synthetic and endogenous cannabinoids has an influence on multiple physiological and pathological processes within the eye.”

http://www.ncbi.nlm.nih.gov/pubmed/19195174

Tetrahydrocannabinol (THC) interferes with conditioned retching in Suncus murinus: an animal model of anticipatory nausea and vomiting (ANV).

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“Little is understood about effective countermeasures to the expression of anticipatory nausea and vomiting (ANV) in chemotherapy patients.

We present a model of ANV based on the emetic reactions of the Suncus murinus (musk shrew). Following two pairings of a novel distinctive contextual cue with the emetic effects of an injection of lithium chloride, the context acquired the potential to elicit retching in the absence of the toxin.

The expression of this conditioned retching reaction was completely suppressed by pretreatment with THC at a dose that did not suppress general activity.

This provides the first experimental evidence in support of anecdotal reports that THC suppresses ANV.”

http://www.ncbi.nlm.nih.gov/pubmed/11277577

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

Delta-9-tetrahydrocannabinol and cannabidiol, but not ondansetron, interfere with conditioned retching reactions elicited by a lithium-paired context in Suncus murinus: An animal model of anticipatory nausea and vomiting.

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“Chemotherapy patients report not only acute nausea and vomiting during the treatment itself, but also report anticipatory nausea and vomiting upon re-exposure to the cues associated with the treatment.

We present a model of anticipatory nausea based on the emetic reactions of the Suncus murinus (musk shrew). Following three pairings of a novel distinctive contextual cue with the emetic effects of an injection of lithium chloride, the context acquired the potential to elicit conditioned retching in the absence of the toxin.

The expression of this conditioned retching reaction was completely suppressed by pretreatment with each of the principal cannabinoids found in marijuana, Delta(9)-tetrahydrocannabinol or cannabidiol, at a dose that did not suppress general activity.

These results support anecdotal claims that marijuana, but not ondansetron, may suppress the expression of anticipatory nausea.”

http://www.ncbi.nlm.nih.gov/pubmed/16197970

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

Cannabinoid agonists and antagonists modulate lithium-induced conditioned gaping in rats.

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“A series of experiments evaluated the potential of psychoactive cannabinoid agonists, delta-9-THC and HU-210, and non-psychoactive cannabinoids, Cannabidiol (CBD) and its dimethylheptyl homolog (CBD-dmh), to interfere with the establishment and the expression of conditioned gaping in rats.

All agents attenuated both the establishment and the expression of conditioned gaping.

Furthermore, the CB1 antagonist, SR-141716, reversed the suppressive effect of HU-210 on conditioned gaping.

Finally, SR-141716 potentiated lithium-induced conditioned gaping, suggesting that the endogenous cannabinoid system plays a role in the control of nausea.”

http://www.ncbi.nlm.nih.gov/pubmed/14527182

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