A physiologically inactive constituent of Cannabis sativa L.
Compound isolated from Cannabis sativa extract.
Compounds having the cannabinoid structure. They were originally extracted from Cannabis sativa L. The most pharmacologically active constituents are TETRAHYDROCANNABINOL; CANNABINOL; and CANNABIDIOL.
The plant genus in the Cannabaceae plant family, Urticales order, Hamamelidae subclass. The flowering tops are called many slang terms including pot, marijuana, hashish, bhang, and ganja. The stem is an important source of hemp fiber.
A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound.
A class of G-protein-coupled receptors that are specific for CANNABINOIDS such as those derived from CANNABIS. They also bind a structurally distinct class of endogenous factors referred to as ENDOCANNABINOIDS. The receptor class may play a role in modulating the release of signaling molecules such as NEUROTRANSMITTERS and CYTOKINES.
Detection of drugs that have been abused, overused, or misused, including legal and illegal drugs. Urine screening is the usual method of detection.

Are cannabinoids detected in hair after washing with Cannabio shampoo? (1/25)

Today, cannabis plants are used in shampoo preparations, in foodstuffs (e.g., oils, noodles, crackers, etc.), and in beverages (e.g., tea). These products often contain < 1% delta9-tetrahydrocannabinol (THC) in order to eliminate psychoactive effects, but some of them can include 1 to 3% of THC. Gas chromatography-mass spectrometry (GC-MS) analysis of Cannabio shampoo revealed the presence of THC (412 ng/mL) and two constituents of cannabis plants, cannabidiol (CBD, 4079 ng/mL) and cannabinol (CBN, 380 ng/mL). In order to verify if normal hygiene practices with Cannabio shampoo can result in positive tests for cannabinoids in hair, three subjects washed their hair with this shampoo once daily for two weeks. After this period, hair specimens were collected. In the three hair specimens, THC, CBD, and CBN were never detected within their limits of detection, 0.05, 0.02, and 0.01 ng/mg, respectively. We concluded that the use of Cannabio shampoo during normal hygiene practices cannot be considered as a source of potential contamination of hair. In a second experiment, drug-free hair specimens (200 mg) were incubated in 10 mL water/Cannabio shampoo (20:1, v/v) for 30 min, 2 h, and 5 h. After incubation, hair strands were washed with water and separated into two portions. One portion was extracted directly; the second was decontaminated with methylene chloride and then extracted. After an incubation period of 30 min, the analysis of hair by GC-MS did not reveal the presence of THC, CBD, and CBN in hair, regardless of whether the hair was decontaminated. After an incubation period of 2 h, specimens tested positive for CBD (0.11 ng/mg without decontamination and 0.10 ng/mg with decontamination) and CBN (0.02 ng/mg without decontamination and 0.02 ng/mg after decontamination). After an incubation period of 5 h, specimens tested positive for CBD (0.25 ng/mg without decontamination and 0.14 ng/mg after decontamination) and CBN (0.02 ng/mg without decontamination and 0.02 ng/mg after decontamination). In all cases, THC was never detected. Extensive but unrealistic use of Cannabio shampoo can cause drug-free hair to test positive for CBD and CBN but not for the primary psychoactive drug THC.  (+info)

Cannabinol-mediated inhibition of nuclear factor-kappaB, cAMP response element-binding protein, and interleukin-2 secretion by activated thymocytes. (2/25)

Cannabinol (CBN), an immunosuppressive cannabinoid and ligand for the peripheral cannabinoid receptor CB2, inhibits the cAMP signaling cascade in forskolin-stimulated thymocytes. The objective of the present studies was to further characterize the mechanism of CBN immune modulation by investigating its effects on interleukin-2 (IL-2) secretion, cAMP response element (CRE), and kappaB DNA binding activity in phorbol ester (phorbol-12-myristate-13-acetate, PMA) plus calcium ionophore (PMA/Io)-activated thymocytes. PMA/Io treatment induced CRE and kappaB DNA binding activity that was attenuated in the presence of CBN. A concomitant and concentration-related inhibition of IL-2 also was produced by CBN in PMA/Io-activated thymocytes. PMA/Io induced two CRE DNA binding complexes, a major complex consisting of a cAMP response element-binding protein (CREB)-1 homodimer, and a minor CREB-1/activating transcription factor (ATF)-2 complex. Both CRE complexes were inhibited by CBN. Conversely, two kappaB DNA binding complexes were observed, but only one was PMA/Io-inducible. However, the DNA binding activity of both complexes was diminished in the presence of CBN. The PMA/Io-inducible kappaB complex was a p65/c-Rel heterodimer. Analysis of up-stream regulation revealed a decrease in phosphorylated CREB/ATF nuclear proteins in PMA/Io-activated thymocytes after CBN treatment. Similarly, CBN prevented the phosphorylation-dependent degradation of the nuclear factor-kappaB inhibitory protein IkappaB-alpha. These results provide a potential link between the CBN-mediated inhibition of thymocyte function, including IL-2 production, and the inhibition of two critical transcription factor families, CREB/ATF and NF-kappaB/Rel.  (+info)

Role of nuclear factor of activated T-cells and activator protein-1 in the inhibition of interleukin-2 gene transcription by cannabinol in EL4 T-cells. (3/25)

We previously reported that immunosuppressive cannabinoids inhibited interleukin (IL)-2 steady-state mRNA expression and secretion by phorbol-12-myristate-13-acetate plus ionomycin-activated mouse splenocytes and EL4 murine T-cells. Here we show that inhibition of IL-2 production by cannabinol, a modest central nervous system-active cannabinoid, is mediated through the inhibition of IL-2 gene transcription. Moreover, electrophoretic mobility shift assays demonstrated that cannabinol markedly inhibited the DNA binding activity of nuclear factor of activated T-cells (NF-AT) and activator protein-1 (AP-1) in a time- and concentration-dependent manner in activated EL4 cells. The inhibitory effects produced by cannabinol on AP-1 DNA binding were quite transient, showing partial recovery by 240 min after cell activation and no effect on the activity of a reporter gene under the control of AP-1. Conversely, cannabinol-mediated inhibition of NF-AT was robust and sustained as demonstrated by an NF-AT-regulated reporter gene. Collectively, these results suggest that decreased IL-2 production by cannabinol in EL4 cells is due to the inhibition of transcriptional activation of the IL-2 gene and is mediated, at least in part, through a transient inhibition of AP-1 and a sustained inhibition of NF-AT.  (+info)

AP-1 activity is negatively regulated by cannabinol through inhibition of its protein components, c-fos and c-jun. (4/25)

Regulation of the activator protein-1 (AP-1) complex is very intricate because it involves phosphorylation state, protein-protein, and protein-DNA interactions. In these studies, the regulation of AP-1 activity, with emphasis on c-fos and c-jun regulation, was investigated using cannabinol (CBN) in primary mouse splenocytes in vitro. Cannabinoid compounds exhibit immunosuppressive actions that are putatively mediated through Gi-protein coupled receptors that negatively regulate adenylate cyclase. However, recent studies suggest that cannabinoids modulate other signaling cascades. Indeed, we demonstrate that CBN inhibited binding to AP-1-containing sites from the interleukin-2 promoter. This inhibition of binding was, in part, due to decreased nuclear expression of c-fos and c-jun. We further determined that the effects of CBN were due to posttranslational modifications of these phosphoproteins and showed that CBN inhibited the activation of ERK MAP kinases. Thus, cannabinoid-induced immunosuppression involves disruption of the ERK signaling cascade.  (+info)

Cannabinoid CB1-receptor mediated regulation of gastrointestinal motility in mice in a model of intestinal inflammation. (5/25)

1. We have studied the effect of cannabinoid agonists (CP 55,940 and cannabinol) on intestinal motility in a model of intestinal inflammation (induced by oral croton oil in mice) and measured cannabinoid receptor expression, endocannabinoids (anandamide and 2-arachidonylglycerol) and anandamide amidohydrolase activity both in physiological and pathophysiological states. 2. CP 55,940 (0.03 - 10 nmol mouse(-1)) and cannabinol (10 - 3000 nmol mouse(-1)) were more active in delaying intestinal motility in croton oil-treated mice than in control mice. These inhibitory effects were counteracted by the selective cannabinoid CB(1) receptor antagonist SR141716A (16 nmol mouse(-1)). SR141716A (1 - 300 nmol mouse(-1)), administered alone, increased intestinal motility to the same extent in both control and croton oil-treated mice. 3. Croton oil-induced intestinal inflammation was associated with an increased expression of CB(1) receptor, an unprecedented example of up-regulation of cannabinoid receptors during inflammation. 4. High levels of anandamide and 2-arachidonylglycerol were detected in the small intestine, although no differences were observed between control and croton oil-treated mice; by contrast anandamide amidohydrolase activity increased 2 fold in the inflamed small intestine. 5. It is concluded that inflammation of the gut increases the potency of cannabinoid agonists possibly by 'up-regulating' CB(1) receptor expression; in addition, endocannabinoids, whose turnover is increased in inflamed gut, might tonically inhibit intestinal motility.  (+info)

Cannabinol enhancement of interleukin-2 (IL-2) expression by T cells is associated with an increase in IL-2 distal nuclear factor of activated T cell activity. (6/25)

It has been demonstrated previously that cannabinol (CBN) differentially modulates interleukin-2 (IL-2) protein secretion by T cells with a corresponding change in extracellular signal-regulated kinase activity. The objective of the present studies was to further investigate the molecular mechanism by which CBN enhances IL-2 gene expression using the EL4 T cell line. We demonstrate here that steady-state IL-2 mRNA expression was significantly enhanced by CBN in a concentration-dependent manner in EL4 cells activated with suboptimal concentrations of phorbol-12-myristate-13-acetate (2-10 nM). Concordantly, a marked increase was observed in nuclear factor of activated T cells (NF-AT) DNA binding activity to the IL-2 distal NF-AT site, but not to nuclear factor for immunoglobulin kappa chain in B cells or activator protein 1 motifs. Transient transfection of EL4 cells with a reporter gene under the control of multiple IL-2 distal NF-AT motifs exhibited increased transcriptional activity by CBN in suboptimally activated cells. In addition, the CBN-mediated enhancement of IL-2 protein secretion and the transcriptional activity of the IL-2 distal NF-AT reporter gene was abrogated by the calcium/calmodulin-dependent protein kinase inhibitor KN93, but not by the CB2 receptor antagonist SR144528. Enhancement of IL-2 was also demonstrated with CP55940, Delta(9)-tetrahydrocannabinol, and cannabidiol, thus suggesting that the phenomenon is not unique to CBN. Collectively, these results suggest that increased IL-2 secretion by CBN is mediated through the enhancement of IL-2 gene transcription by activation of NF-AT in a CB1/CB2-independent manner.  (+info)

Delta 9-tetrahydrocannabinol and cannabinol activate capsaicin-sensitive sensory nerves via a CB1 and CB2 cannabinoid receptor-independent mechanism. (7/25)

Although Delta(9)-tetrahydrocannabinol (THC) produces analgesia, its effects on nociceptive primary afferents are unknown. These neurons participate not only in pain signaling but also in the local response to tissue injury. Here, we show that THC and cannabinol induce a CB(1)/CB(2) cannabinoid receptor-independent release of calcitonin gene-related peptide from capsaicin-sensitive perivascular sensory nerves. Other psychotropic cannabinoids cannot mimic this action. The vanilloid receptor antagonist ruthenium red abolishes the responses to THC and cannabinol. However, the effect of THC on sensory nerves is intact in vanilloid receptor subtype 1 gene knock-out mice. The THC response depends on extracellular calcium but does not involve known voltage-operated calcium channels, glutamate receptors, or protein kinases A and C. These results may indicate the presence of a novel cannabinoid receptor/ion channel in the pain pathway.  (+info)

(-)-7'-Isothiocyanato-11-hydroxy-1',1'-dimethylheptylhexahydrocannabinol (AM841), a high-affinity electrophilic ligand, interacts covalently with a cysteine in helix six and activates the CB1 cannabinoid receptor. (8/25)

The CB1 cannabinoid receptor has been shown to play important physiological roles in the central nervous system, as well as peripherally, and is a target for development of therapeutic medications. To gain insight on the ligand binding site(s) and structural features of activation, we designed and synthesized (-)-7'-isothiocyanato-11-hydroxy-1',1'-dimethylheptylhexahydrocannabinol (AM841), a classical cannabinoid affinity label that incorporates an isothiocyanate substituent as an electrophilic reactive group capable of interacting irreversibly with a suitably located and properly oriented nucleophilic amino acid residue at or near the binding site. To obtain evidence for the site of covalent attachment of AM841, C6.47, identified in part by interactive ligand docking, was mutated to serine, alanine, and leucine to reduce or eliminate the nucleophilic character. Wild-type (WT) and mutant CB1 receptors were evaluated for their abilities to recognize a series of cannabinergic ligands. Each bound comparably to WT, excluding C6.47L, which displayed a reduced affinity for 3H-labeled (1R,3R,4R)-3-[2-hydroxy-4-(1,1-dimethylheptyl)phenyl]-4-(3-hydroxypropyl)cyclohex an-1-ol (CP55940), AM841, 11-hydroxy-1',1'-dimethylheptylhexahydrocannabinol (AM4056), and (-)-7'-bromo-11-hydroxy-1',1'-dimethylheptylhexahydrocannabinol (AM4043) and an improvement in affinity for (-)-trans-delta9-tetrahydrocannabinol (delta9-THC). The affinity of 3H-labeled [2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrrolo-[1,2,3-de]-1,4-benzoxazin- 6-yl](naphthyl)methanone (WIN55212-2) was unchanged across all mutants. It is noteworthy that AM841 was shown to bind irreversibly to WT CB1 but exhibited no covalent attachment with the mutants and behaved as an agonist suggesting irreversible attachment to C6.47 maintains CB1 in its active state. The evidence presented identifies C6.47 as the site of covalent bond formation with AM841 and combined with the binding data fully supports the molecular modeling. These studies present the first report of tandem applications of affinity labeling, site-directed mutagenesis, and interactive ligand docking for CB1.  (+info)

Cannabinol (CBN) is a chemical compound found in cannabis plants. It is one of the many cannabinoids that can be extracted from the plant, but it is not as well-known or widely studied as tetrahydrocannabinol (THC) and cannabidiol (CBD).

CBN is formed when THC degrades over time due to exposure to air, heat, and light. As a result, older or improperly stored cannabis may contain higher levels of CBN than fresh or properly stored cannabis.

CBN has been shown to have some therapeutic potential, including as a sedative, an anti-inflammatory, and an appetite stimulant. However, more research is needed to fully understand its effects and potential medical uses. It's worth noting that CBN does not produce the psychoactive effects associated with THC.

Cannabidiol (CBD) is a chemical compound found in the Cannabis sativa plant, also known as cannabis or marijuana. It is one of many such compounds, known as cannabinoids, that are found in the plant. Unlike tetrahydrocannabinol (THC), which is the main psychoactive component of cannabis and is responsible for the "high" associated with its use, CBD does not have psychoactive effects.

CBD has been studied for its potential therapeutic uses in a variety of medical conditions, including epilepsy, anxiety, and chronic pain. It is available in various forms, such as oils, capsules, and topical creams, and can be taken orally or applied to the skin. However, it is important to note that the use of CBD is not currently approved by the U.S. Food and Drug Administration (FDA) for the treatment of any medical condition, except for the treatment of certain forms of epilepsy. As with any medication or supplement, it is important to talk to your doctor before using CBD, especially if you are taking other medications or have underlying health conditions.

Cannabinoids are a class of chemical compounds that are produced naturally in the resin of the cannabis plant (also known as marijuana). There are more than 100 different cannabinoids that have been identified, the most well-known of which are delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD).

THC is the primary psychoactive component of cannabis, meaning it is responsible for the "high" or euphoric feeling that people experience when they use marijuana. CBD, on the other hand, does not have psychoactive effects and is being studied for its potential therapeutic uses in a variety of medical conditions, including pain management, anxiety, and epilepsy.

Cannabinoids work by interacting with the body's endocannabinoid system, which is a complex network of receptors and chemicals that are involved in regulating various physiological processes such as mood, appetite, pain sensation, and memory. When cannabinoids bind to these receptors, they can alter or modulate these processes, leading to potential therapeutic effects.

It's important to note that while some cannabinoids have been shown to have potential medical benefits, marijuana remains a controlled substance in many countries, and its use is subject to legal restrictions. Additionally, the long-term health effects of using marijuana or other forms of cannabis are not fully understood and are the subject of ongoing research.

Cannabis is a plant genus that includes three species: Cannabis sativa, Cannabis indica, and Cannabis ruderalis. It contains psychoactive compounds called cannabinoids, the most notable of which is delta-9-tetrahydrocannabinol (THC), which produces the "high" associated with marijuana use.

Cannabis sativa and Cannabis indica are primarily used for recreational and medicinal purposes, while Cannabis ruderalis has a lower THC content and is mainly used for industrial purposes, such as hemp fiber production.

Medicinally, cannabis is used to treat various conditions, including pain, nausea, and loss of appetite associated with cancer and HIV/AIDS, multiple sclerosis, epilepsy, and post-traumatic stress disorder (PTSD), among others. However, its use remains controversial due to its psychoactive effects and potential for abuse. Its legal status varies widely around the world, ranging from outright prohibition to decriminalization or full legalization for medical and/or recreational purposes.

Dronabinol is a synthetic form of delta-9-tetrahydrocannabinol (THC), which is the main psychoactive compound found in cannabis. It is approved by the US Food and Drug Administration (FDA) for the treatment of nausea and vomiting caused by chemotherapy in cancer patients, as well as to stimulate appetite and weight gain in patients with AIDS wasting syndrome.

Dronabinol is available in capsule form and is typically taken two to three times a day, depending on the prescribed dosage. It may take several days or even weeks of regular use before the full therapeutic effects are achieved.

Like cannabis, dronabinol can cause psychoactive effects such as euphoria, altered mood, and impaired cognitive function. Therefore, it is important to follow the prescribing instructions carefully and avoid driving or operating heavy machinery while taking this medication. Common side effects of dronabinol include dizziness, drowsiness, dry mouth, and difficulty with coordination.

Cannabinoid receptors are a class of cell membrane receptors in the endocannabinoid system that are activated by cannabinoids. The two major types of cannabinoid receptors are CB1 receptors, which are predominantly found in the brain and central nervous system, and CB2 receptors, which are primarily found in the immune system and peripheral tissues. These receptors play a role in regulating various physiological processes such as appetite, pain-sensation, mood, and memory. They can be activated by endocannabinoids (cannabinoids produced naturally in the body), phytocannabinoids (found in cannabis plants), and synthetic cannabinoids.

Substance abuse detection refers to the process of identifying the use or misuse of psychoactive substances, such as alcohol, illicit drugs, or prescription medications, in an individual. This can be done through various methods, including:

1. Physical examination: A healthcare professional may look for signs of substance abuse, such as track marks, enlarged pupils, or unusual behavior.
2. Laboratory tests: Urine, blood, hair, or saliva samples can be analyzed to detect the presence of drugs or their metabolites. These tests can provide information about recent use (hours to days) or longer-term use (up to several months).
3. Self-report measures: Individuals may be asked to complete questionnaires or interviews about their substance use patterns and behaviors.
4. Observational assessments: In some cases, such as in a treatment setting, healthcare professionals may observe an individual's behavior over time to identify patterns of substance abuse.

Substance abuse detection is often used in clinical, workplace, or legal settings to assess individuals for potential substance use disorders, monitor treatment progress, or ensure compliance with laws or regulations.

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Cannabinol (CBN). Meaning. Cannabinol (CBN) is the non-intoxicating cannabis compound that exists in most strains. It is like ...
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|h2||span|Soothes Tremors|/span||/h2| |p||span|The effects of cannabis have been shown to reduce pain and tremors, and improve sleep for those who have Parkinson’s disease. There has also been research that demonstrated improved fine motor skills among its patients.|/span||/p| |h2||span|Relieves Anxiety and Stress|/span||/h2| |p||span|One of the most popular and well-known uses of cannabis oil is for the purpose of relief from anxiety and stress. The natural compounds found in cannabis oil are effective for releasing relaxing the mind, releasing pleasure hormone, reducing stress and inducing a sense of calmness and relaxation to the user|/span||/p| |h2||span|Treats PTSD|/span||/h2| |p||span|The naturally occurring cannabinoids, similar to THC, contribute to the health benefits of cannabis oil. The cannabinoids help to regulate the system that causes anxiety and fear in the brain and body. This specific use of |a href=https://herbalganjadispensary.com/product/a1-meds-cart/|a1 meds carts
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The Journal Club: Cannabinol (CBN) & Mitochondrial Function. by Csequence , Aug 3, 2022 , Communications , 0 comments ... Sitbon discuss the potential use of a lesser known cannabinoid called cannabinol (CBN) in inhibiting oxytosis/ferroptosis via ... Discussion around the effects of cannabinol administration on oxytososis/ferroptosis via regulation of mitochondrial function. ... "Cannabinol inhibits oxytosis/ferroptosis by directly targeting mitochondria independently of cannabinoid receptors", in which ...
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1.7.5 Cannabinol (CBN). *1.7.6 Tetrahydrocannabinol (THC). *1.8 Terpenoids *1.8.1 α-Bisabolol ...
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This is a Beginners Guide to Cannabinol. CBN is the byproduct of THC that has been aged. It triggers the CB1 and CB2 receptors. ... Few, if any, countries have passed laws particularly for Cannabinol. As a result of this, Cannabinol becomes governed under the ... Cannabinol also forms in the body when THC is passed through the metabolic process.. Not unlike THC, CBN may trigger the CB1 ... Cannabinol carries some features of THC and some see it as a bit of a hybrid between CBD and THC. However, when compared with ...
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