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Cbd cannabis oil reviews 2016

Receptor CB1 Activation Cells CBD Reduces in

zerobg
09.06.2018

Content:

  • Receptor CB1 Activation Cells CBD Reduces in
  • Cannabinoids, Endocannabinoids and Cancer
  • CB1 and CB2 Receptors Are The Most Common
  • 5-HT1A is a member of the family of 5-HT receptors, which are activated by the receptor. Anandamide, the endogenous cannabinoid, is also a TRPV1 agonist. CBD may act to decrease both bone reabsorption and cancer cell proliferation. We aim to define several potential roles of cannabinoid receptors in . Once endocannabinoids are taken up by the cells, they can be . reduces neuronal firing through the opening of Ca2+-activated .. The drug with brand name Sativex, containing equal amount of THC and CBD, is used to treat several. Binding to the CB1 receptor is responsible for the analgesic activity of . Up- regulation of the CB1 gene is mediated by IL-4 release and activation of the Cannabidiol reduces the invasiveness of breast cancer cells by inhibiting Id

    Receptor CB1 Activation Cells CBD Reduces in

    In prostate cancer, CB1 receptor expression by the human prostate cancer cell lines LNCaP androgen-sensitive , DU and PC3 androgen-independent are higher than that seen in normal human prostate epithelial cells [ 46 ].

    This was confirmed in prostate carcinoma specimens where expression of the CB1 and TRPV1 receptors are up-regulated and correlate with increasing tumor grades [ 47 ]. It has also been shown that the level of CB1 in tumor tissue is associated with disease severity at diagnosis and outcome [ 48 ]. In pancreatic tumors high CB1 receptor expression is associated with a shorter survival time median 6 months than low CB1 expression median 16 months in humans [ 30 ].

    In contrast, in hepatocellular carcinoma, over-expression of CB1 and CB2 receptors are correlated with improved prognosis in humans [ 49 ]. In addition to signaling through cannabinoid receptors, cannabinoids, in particular anandamide and cannabidiol, have CB receptor-independent effects. AEA has been shown to induce neuroblastoma, lymphoma, and uterine cervix carcinoma cell death through vanilloid receptors [ 51 , 52 ].

    It has also been proposed that lipid rafts, membrane domains rich in sphingolipids and cholesterol, mediate AEA effects through CB1 signaling [ 53 , 54 ]. In cholangiocarcinoma, the anti-proliferative and pro-apoptotic action of AEA is facilitated by lipid raft stabilization, ceramide accumulation, and recruitment of FAS and FAS ligand into lipid rafts [ 55 ].

    Another cellular protein that may be important in CB receptor-independent cell death induced by endocannabinoids is COX In human neuroblastoma and C6 glioma cells AEA induces apoptosis through a vanilloid receptor mediated increase in intracellular calcium concentration, which activates COX-2, releases cytochrome c and activates caspase 3 [ 52 ].

    An important molecule for studying cannabinoid receptor-independent effects is cannabidiol. Cannabidiol is a cannabinoid analog that has no activity at CB1 or CB2 receptors and lacks psychotropic effects. Cannabidiol has been shown to inhibit glioma and breast tumor growth in vitro and in vivo through induction of apoptosis and inhibition of cell migration and angiogenesis, with these effects being independent of CB and TRPV1 receptor activity [ 60 - 62 ].

    Cannabidiol reduces the invasiveness of breast cancer cells by inhibiting Id-1, an inhibitor of basic helix-loop-helix transcription factors involved in tumor progression, at the promoter level [ 63 ].

    A quinone analog of cannabidiol, HU, a highly specific inhibitor of topoisomerase II, has been reported to have high efficacy against human cancer cell lines in vitro and against tumor grafts in nude mice [ 64 ]. HU also inhibits angiogenesis by directly inducing apoptosis of vascular endothelial cells without changing the expression of pro- and anti-angiogenic cytokines and their receptors [ 65 ]. Cannabinoids have been shown to cause cell cycle arrest in various cancer cell lines.

    However, CB2-selective antagonists significantly, but not totally, prevent these effects, suggesting a contribution of a CB2 receptor-independent mechanism [ 68 ].

    WIN, treatment of LNCaP cells also causes a dose-dependent decrease in the expression of cyclin D1, cyclin D2 and cyclin E, as well as cdk2, cdk4 and cdk6, pRb and its molecular partner, the transcription factor E2F [ 69 ]. WIN, causes a dose-dependent decrease in the protein expression of DP-1 and DP-2, which form heterodimeric complexes with E2F essential for activity [ 69 ]. CB1 also reduces cyclic AMP-dependent protein kinase A signaling leading to down-regulation of the anti-apoptotic factor survivin [ 45 ].

    Survivin over-expression is associated with poor clinical outcomes and reduced tumor apoptosis in patients with colorectal cancer [ 73 , 74 ]. Survivin is an attractive target for pharmacological modulation because it is over-expressed in most human tumors but is present in very small amounts in normal adult tissues [ 74 ]. A direct link between CB1 activation and decreased survivin expression has been established through treatment of SW cells with AM, a CB1 receptor agonist [ 19 ].

    Activation of CB1 or CB2 receptors has been shown to stimulate de novo synthesis of ceramide in human tumors including glioma, leukemia, and pancreatic, and DLD-1 and HT29 colorectal cancer cells [ 75 - 77 ]. Ceramide is a pro-apoptotic lipid that causes up-regulation of the stress protein p8 and several downstream stress-related genes expressed in the endoplasmic reticulum including ATF-4, CHOP, and TRB3 [ 78 ]. In DLD-1 and HT29 colorectal cancer cells, CB1 and CB2 receptor activation leads to increased ceramide levels, whereas CB1 and CB2 receptor-induced apoptosis is prevented by the pharmacologic inhibition of de novo ceramide synthesis [ 77 ].

    A role for Bcl-2 family members, such as Bad, has also been hypothesized in cannabinoid-dependent apoptosis [ 81 ]. Pro-apoptotic effects may rely also on a CB1 receptor-independent stimulation of sphingomyelin breakdown [ 84 ].

    A common event in cannabinoid-induced apoptosis is the depolarization of mitochondria via cytochrome c release [ 85 - 87 ]. CB agonists have been reported to be mitochondrial inhibitors, since they decrease oxygen consumption and mitochondrial membrane potential while increasing mitochondrial hydrogen peroxide production, thus inducing apoptosis [ 88 ]. AEA inhibits breast cancer cell proliferation through down-regulation of the prolactin receptor, brca1 gene product, and the high affinity neurotrophins receptor trk [ 89 , 93 ].

    The anti-proliferative effect of AEA is proportional to the degree of hormone dependency of the cell lines and the mechanism relies on the inhibition of the cAMP-dependent PKA pathway [ 93 ]. These effects are CB1-mediated [ 91 ]. Similar growth arrest and receptor modulation by AEA are observed in prolactin and nerve growth factor-stimulated DU cells [ 92 - 94 ]. Treatment of LNCaP cells with WIN, results in decreased proliferation, androgen receptor expression, VEGF protein expression, and secreted levels of PSA, a glycoprotein androgen receptor-regulated protein that is a marker of prostate cancer progression [ 46 ].

    The antagonistic effect of endocannabinoids on growth factor-induced proliferation has also been reported in glioma [ 95 ]. Cannabinoids have been shown to inhibit tumor growth by lowering vascular density in tumors.

    Cannabinoids cause a lower distribution of CDpositive cells, a common angiogenesis marker, in experimental tumor xenografts from glioma, melanoma and nonmelanoma skin cancer, and lung tumor cells [ 32 , 96 - 98 ]. Met-fluoro-anandamide Met-F-AEA , a metabolically stable analog of AEA, has been demonstrated to reduce the sprout number and length of endothelial cell spheroids, inhibit capillary-like tube formation in vitro , and suppress angiogenesis in an in vivo chick chorioallantoic membrane assay [ 99 ].

    Furthermore, experimental tumors from animals treated with cannabinoids have been shown to exert a vascular network that is small, undifferentiated, and impermeable giving tumors a paler appearance when compared to controls [ 90 , 96 ]. In addition to the direct inhibition of vascular endothelial cell migration and survival, cannabinoids decrease the expression of proangiogenic factors in tumors. Several studies have revealed that cannabinoids have an effect on the expression of VEGF, which is one of the major cancer cell-released chemoattractants in tumor neovascularization [ ].

    JWH down-regulates connective tissue growth factor and heme oxygenase-1, genes known to be regulated by VEGF, as well as the VEGF-related factors, inhibitor of differentiation-3 Id-3 , midkine, and the angiopoietin receptor tyrosine kinase with immunoglobulin-like and epidermal growth factor EGF -like domains 1 Tie-1 [ , ]. Cannabinoids diminish the expression of angiopoietin-2 Ang-2 and placental growth factor PlGF along with the appearance of narrow capillaries and a decrease of blood vessel size [ 32 ].

    JWH down-regulates Ang-2, which supports the formation of mature blood vessels, in gliomas and astrocytomas [ 96 , ]. Angiogenesis involves several proteolytic enzymes. THC down-regulates the proangiogenic factor MMP-2 in human tumor samples from recurrent glioblastoma multiforme and in nude mice xenografted with the C6.

    THC and methanandamide decrease MMP-2 expression in vitro in cervical cancer cells accompanied by a reduced invasiveness of the cancer cells [ 45 ]. JWH also decreases MMP-2 expression in vivo in glioma xenografts and impairs tumor vasculature [ 96 ]. The effects of cannabinoids on several antiangiogenic factors have also been studied.

    WIN, and JWH do not have an effect on the expression of thrombospondin-1 and -2, multidomain matrix glycoproteins that inhibit neovascularization, in nude mice xenografted with melanoma carcinoma cells [ 32 ]. The effects of cannabinoids on the expression of TIMP-1, an inhibitor of angiogenesis, are dependent on the specific cancer cell line used [ ]. In human cervical and lung cancer cells, cannabinoids up-regulate TIMP-1 expression and are anti-invasive [ 45 ].

    In contrast, THC down-regulates TIMP-1 in glioma cell lines and in human tumor samples from recurrent glioblastoma multiforme patients [ ]. The cannabinoid derivative HU is antiangiogenic through a different mechanism. HU inhibits angiogenesis by directly inducing apoptosis of vascular endothelial cells without modulating the expression of pro- and antiangiogenic factors and their receptors [ 65 ].

    Tumor cell migration is an important step for the spread of cancer [ ]. As an initial step, the primary tumor has to enter lymphatic or blood vessels.

    Migration of cancer cells is initiated by paracrine or endocrine chemoattractants but is also affected by neurotransmitters and other factors. Among the chemoattractants that trigger migration, cell growth, proliferation, and differentiation, EGF and its receptor, EGFR, play a pivotal role. As described earlier, THC action modulates intracellular signaling events downstream of EGFR, such as inhibition of mitogen-activated protein kinases and protein kinase B Akt activity [ 98 ].

    The impact of cannabinoids on EGFR activation appears to be cell type specific. In glioma and lung carcinoma, cannabinoid receptor agonists induce cell proliferation through cannabinoid-induced EGFR signal transactivation [ ]. Human astrocytoma cells have no change in EGFR tyrosine phosphorylation when treated with cannabinoids [ ]. Neurotransmitters also play a role in regulating cell migration [ ]. Cannabinoids have an inhibitory action on norepinephrine-induced cancer cell migration [ ].

    The pathways involved in CB1-receptor dependent antimigratory effects have been explored in some depth. Mast cells are a source of chemoattractants and are possible targets of cannabinoids [ ]. Cancer cell migration initiated by mast cells is down-regulated by 2-AG and WIN, in the scratch wound healing assay in a CB1-receptor dependent manner [ ]. Human glioma cell migration is inhibited by cannabidiol in a receptor-independent manner, as evidenced by the failure of cannabinoid receptor antagonists and pertussis toxin to reverse the antimigratory action of cannabidiol [ 61 ].

    AM and THC do not affect the basal migration of human cervical and lung cancer cells, implicating a cell type-specific or chemoattractant-dependent regulation of migration by cannabinoids [ 45 ]. Thus, cannabinoids are antimigratory in some cancer cell lines but the underlying signaling pathways are not fully elucidated.

    The adhesive interaction of tumor cells with the surrounding microenvironment is a critical factor in their growth, migration and metastasis. Matrix proteins such as integrins, cadherins, selectins, and cell adhesion molecules of the immunoglobulin superfamily IgSF CAMs are integral to the adhesion of tumor cells to the extracellular matrix ECM. Cannabinoids have been shown to have various effects on the adhesion of tumors cells to the ECM. Met-F-AEA selectively reduces the adhesion of human breast cancer cells to the ECM component collagen type IV in a CB1 receptor-dependent manner in vitro , but has no effect on adhesion to fibronectin and laminin [ ].

    Met-F-AEA does not affect the expression of integrins but it does decrease their affinity for collagen through suppression of phosphorylation of the focal adhesion kinase FAK and the pro-oncogenic tyrosine kinase Src [ ]. HU does not have a direct effect on FAK phosphorylation in murine neuroblastoma cells [ ]. WIN, blocks the interleukin 1 IL-1 -induced up-regulation of intercellular cell adhesion molecule 1 and vascular cell adhesion molecule 1- two IgSF CAMs- in human glioblastoma and lymphoma cells in a cannabinoid receptor-independent manner [ ].

    Cancer cell invasion is one of the crucial events in local spreading, growth, and metastasis of tumors. However, the precise mechanism leading to decreased invasiveness by cannabinoids has not been fully elucidated. Several investigations have provided insight into how cannabinoids may achieve their anti-invasive action.

    Cannabinoids have been shown to modulate the MMP system, which, in part, leads to their anti-invasive action. MMPs degrade ECM components, an important function in tumor invasion, metastasis, and angiogenesis [ , ]. Cannabinoids have been shown to have a direct effect on the MMP system.

    JWH decreases the expression and activity of MMP-2 in mice xenografted with a rat glioma cell line and human grade IV astrocytoma cells [ 96 ]. Cannabinoid-induced inhibition of MMP-2 expression and cell invasion is prevented by blocking ceramide biosynthesis and by knocking down the expression of the stress protein p8 [ ]. There is a correlation between high cancer invasiveness and decreased TIMP-1 expression; in addition, the anti-invasive action of several drugs has been associated with elevated TIMP-1 levels [ - ].

    In glioma cell lines and primary tumor cells from glioblastoma multiforme tissues, TIMP-1 expression is inhibited by cannabinoids [ ]. Instead, the cannabinoid-induced apoptosis is dependent on de novo synthesis of ceramide [ ]. Thus, cannabinoid action on TIMP-1 expression and the subsequent impact on tumorigenesis depends on tumor type. In vivo studies demonstrate that cannabinoids reduce tumor growth and metastasis as well as cell proliferation and angiogenesis in mice.

    THC decreases tumor size, number of tumor and lung metastases, and inhibits both cell proliferation and angiogenesis in an animal model of metastatic breast cancer [ ]. This inhibition of cell proliferation involves CB2 but not CB1 receptors [ ]. Structure of a cannabinoid receptor and functional expression of the cloned cdna. Determination and characterization of a cannabinoid receptor in rat brain.

    International union of basic and clinical pharmacology. Cannabinoid receptors and their ligands: Beyond CB1and CB 2. Molecular characterization of a peripheral receptor for cannabinoids. Endocannabinoid-mediated control of synaptic transmission.

    International union of pharmacology. Classification of cannabinoid receptors. Identification of an endogenous 2-monoglyceride, present in canine gut, that binds to cannabinoid receptors. Isolation and structure of a brain constituent that binds to the cannabinoid receptor. New therapeutic opportunities from an ancient herb. Phytocannabinoids as novel therapeutic agents in cns disorders. Cannabinoids in models of chronic inflammatory conditions. Phytocannabinoids for cancer therapeutics: Recent updates and future prospects.

    The first 66 years. Associations between cannabinoid receptor-1 CNR1 variation and hippocampus and amygdala volumes in heavy cannabis users. The association between cannabinoid receptor 1 gene CNR1 and cannabis dependence symptoms in adolescents and young adults. Candidate genes for cannabis use disorders: Findings, challenges and directions. Crystal structure of the human cannabinoid receptor CB1. High-resolution crystal structure of the human CB1cannabinoid receptor.

    Crystal structures of agonist-bound human cannabinoid receptor CB1. Identification and characterisation of a novel splice variant of the human CB1receptor. An amino-terminal variant of the central cannabinoid receptor resulting from alternative splicing.

    Differential signalling in human cannabinoid CB1 receptors and their splice variants in autaptic hippocampal neurones. Similar in vitro pharmacology of human cannabinoid CB1 receptor variants expressed in cho cells. Species differences in cannabinoid receptor 2 and receptor responses to cocaine self-administration in mice and rats.

    Species differences in cannabinoid receptor 2 CNR2 gene: Identification of novel human and rodent CB2 isoforms, differential tissue expression and regulation by cannabinoid receptor ligands.

    Why do cannabinoid receptors have more than one endogenous ligand? Endocannabinoid signaling and synaptic function. Endocannabinoid signaling as a synaptic circuit breaker in neurological disease.

    A novel hepatic endocannabinoid and cannabinoid binding protein. A comprehensive profile of brain enzymes that hydrolyze the endocannabinoid 2-arachidonoylglycerol. Endocannabinoid oxygenation by cyclooxygenases, lipoxygenases, and cytochromes p Cross-talk between the eicosanoid and endocannabinoid signaling pathways.

    Anandamide inhibits metabolism and physiological actions of 2-arachidonoylglycerol in the striatum. Endocannabinoid-mediated retrograde modulation of synaptic transmission.

    Anandamide, cannabinoid type 1 receptor, and nmda receptor activation mediate non-hebbian presynaptically expressed long-term depression at the first central synapse for visceral afferent fibers.

    Polymodal activation of the endocannabinoid system in the extended amygdala. Trpv1 activation by endogenous anandamide triggers postsynaptic long-term depression in dentate gyrus.

    Postsynaptic trpv1 triggers cell type-specific long-term depression in the nucleus accumbens. Rgs4 is required for dopaminergic control of striatal ltd and susceptibility to parkinsonian motor deficits.

    Chronic monoacylglycerol lipase blockade causes functional antagonism of the endocannabinoid system. The endocannabinoid 2-arachidonoylglycerol is responsible for the slow self-inhibition in neocortical interneurons. Diacylglycerol lipase is not involved in depolarization-induced suppression of inhibition at unitary inhibitory connections in mouse hippocampus.

    Self-modulation of neocortical pyramidal neurons by endocannabinoids. Long-lasting self-inhibition of neocortical interneurons mediated by endocannabinoids. Acute cannabinoids impair working memory through astroglial CB1 receptor modulation of hippocampal ltd. Endocannabinoids potentiate synaptic transmission through stimulation of astrocytes. Endocannabinoids mediate neuron-astrocyte communication. Endocannabinoid signaling in microglial cells.

    CB2 cannabinoid receptors as a therapeutic target-what does the future hold? A cannabinoid receptor with an identity crisis. Immunohistochemical localization in rat brain. Excitability of prefrontal cortical pyramidal neurons is modulated by activation of intracellular type-2 cannabinoid receptors.

    Distribution of cannabinoid receptors in the central and peripheral nervous system. Presynaptically located CB1 cannabinoid receptors regulate GABA release from axon terminals of specific hippocampal interneurons.

    Immunohistochemical distribution of cannabinoid CB1 receptors in the rat central nervous system. Cannabinoid control of learning and memory through hcn channels. Endocannabinoid signaling at the periphery: The cannabinoid CB1 receptor regulates bone formation by modulating adrenergic signaling.

    Anandamide suppresses pain initiation through a peripheral endocannabinoid mechanism. The neuronal distribution of cannabinoid receptor type 1 in the trigeminal ganglion of the rat. Characterisation of cannabinoid 1 receptor expression in the perikarya, and peripheral and spinal processes of primary sensory neurons.

    Cannabinoids and the gut: New developments and emerging concepts. The highs and lows of cannabinoid receptor expression in disease: Mechanisms and their therapeutic implications. At the heart of the matter: The endocannabinoid system in cardiovascular function and dysfunction. Type I cannabinoid receptor trafficking: All roads lead to lysosome. Constitutive endocytic cycle of the CB1 cannabinoid receptor.

    Cannabinoid receptor 1 trafficking and the role of the intracellular pool: Regulation of CB1 cannabinoid receptor trafficking by the adaptor protein ap Intracellular cannabinoid type 1 CB 1 receptors are activated by anandamide. Cellular effects of cannabinoids. Mitochondrial CB1 receptors regulate neuronal energy metabolism.

    Cannabinoid control of brain bioenergetics: Exploring the subcellular localization of the CB1 receptor. Studying mitochondrial CB1 receptors: A tale of two methods: Identifying neuronal CB1 receptors. Hypothalamic pomc neurons promote cannabinoid-induced feeding. Mitochondrial CB1 receptor is involved in acea-induced protective effects on neurons and mitochondrial functions.

    A cannabinoid link between mitochondria and memory. Mitochondrial transport in neurons: Impact on synaptic homeostasis and neurodegeneration. Mitochondria in neuroplasticity and neurological disorders. Activation-dependent subcellular distribution patterns of CB1 cannabinoid receptors in the rat forebrain.

    Differential activation of intracellular versus plasmalemmal CB2 cannabinoid receptors. Cannabinoid receptor activation differentially regulates the various adenylyl cyclase isozymes. Paradoxical action of the cannabinoid win 55, in stimulated and basal cyclic amp accumulation in rat globus pallidus slices.

    Concurrent stimulation of cannabinoid CB1 and dopamine d2 receptors augments camp accumulation in striatal neurons: Evidence for a gs linkage to the CB1 receptor. Dual activation and inhibition of adenylyl cyclase by cannabinoid receptor agonists: Evidence for agonist-specific trafficking of intracellular responses.

    Signal transduction of the CB1 cannabinoid receptor. Endocannabinoids inhibit transmission at granule cell to purkinje cell synapses by modulating three types of presynaptic calcium channels. Anandamide, an endogenous cannabinoid, inhibits calcium currents as a partial agonist in N18 neuroblastoma-cells. Cannabinoids inhibit N-type calcium channels in neuroblastoma glioma-cells.

    Presynaptic calcium channel inhibition underlies CB1 cannabinoid receptor-mediated suppression of gaba release. Cannabinoids modulate the P-type high-voltage-activated calcium currents in purkinje neurons. Cannabinoids activate an inwardly rectifying potassium conductance and inhibit Q-type calcium currents in att20 cells transfected with rat-brain cannabinoid receptor.

    Endocannabinoids modulate N-type calcium channels and G-protein-coupled inwardly rectifying potassium channels via CB1 cannabinoid receptors heterologously expressed in mammalian neurons. Localization and mechanisms of action of cannabinoid receptors at the glutamatergic synapses of the mouse nucleus accumbens. CB1 cannabinoid receptors and their associated proteins. Mechanism of extracellular signal-regulated kinase activation by the CB1 cannabinoid receptor. Ligand-specific endocytic dwell times control functional selectivity of the cannabinoid receptor 1.

    Activation of mitogen-activated protein-kinases by stimulation of the central cannabinoid receptor CB1. Cannabinoids activate p38 mitogen-activated protein kinases through CB1 receptors in hippocampus.

    The CB1 cannabinoid receptor is coupled to the activation of c-jun N-terminal kinase. Functional CB1 cannabinoid receptors in human vascular endothelial cells. Back to the future.

    Desensitization of cannabinoid-mediated presynaptic inhibition of neurotransmission between rat hippocampal neurons in culture. Distinct domains of the CB1 cannabinoid receptor mediate desensitization and internalization. Beta-arrestin2 regulates cannabinoid CB1 receptor signaling and adaptation in a central nervous system region-dependent manner.

    Distinct roles of beta-arrestin 1 and beta-arrestin 2 in orginduced biased signaling and internalization of the cannabinoid receptor 1 CB1 J. Gomez del Pulgar T. Cannabinoids promote oligodendrocyte progenitor survival: Endocannabinoid signalling and the deteriorating brain. Cannabis and the brain. Targeting the endocannabinoid system: To enhance or reduce?

    CB1 cannabinoid receptor inhibits synaptic release of glutamate in rat dorsolateral striatum. A restricted population of CB1 cannabinoid receptors with neuroprotective activity. CB1 cannabinoid receptors and on-demand defense against excitotoxicity. Has beneficial anti-ischemic effects.

    Increases CCK and ghrelin release. Lowers inflammation and permeability in the gut. Bad May participate in tumor formation in the brain. May Interact with circadian rhythm. Impairs memory and increases fatigue.

    Decreases Acetylcholine and glutamine. May contribute to anxiety. May lead to obesity and metabolic disorders. Decreases thyroid hormones TSH mostly. Can affect mitochondrial energy.

    CB2 Good Stimulates of opioid receptor. Regulates lipid production and cell death. Inhibit the release of proinflammatory factors. CB2 is upregulated in autism. Promotes Neurogenesis Recent studies indicate that a natural cannabinoid of cannabis, specifically CBD, increases adult neurogenesis.

    In iron treated rats, chronic cannabidiol improved recognition memory in iron-treated rats. There have been studies showing no efficacy in AD too. Protects the Brain Acute and chronic administration of cannabidiol increases mitochondrial complex and creatine kinase activity in the rat brain.

    CBD rescued iron-induced effects, bringing hippocampal DNM1L, caspase 3, and synaptophysin levels back to values comparable to the control group. Helps with Anxiety CBD was shown to reduce anxiety in patients with social anxiety disorder by inducing activity in limbic and paralimbic brain areas. It also helped with public speaking induced anxiety.

    Stress-induced downregulation of hippocampal eCB signaling. CB1 receptor-endocannabinoid signaling is activated by stress and functions to buffer or dampen the behavioral and endocrine effects of acute stress. May Help with Depression The EC system is suggested to be dysfunctional in mood and related disorders.

    CBD induces antidepressant-like effects comparable to those of imipramine, an anti-depressant. Also, it exhibited an anti-anxiety and antidepressant effects in animal models.

    Acts via enhancing both serotonergic and glutamate cortical signalling through a 5-HT1A receptor-dependent mechanism. Abnormalities in the cannabinoid-1 receptor CNR1 gene that codes for cannabinoid-1 CB1 receptors are reported in psychiatric disorders.

    Has Anti-Inflammatory Properties CB2 receptors are expressed in several types of inflammatory cells and immunocompetent cells. Activating CB2 receptors inhibit the release of proinflammatory factors.

    CB1 and CB2 are expressed by human gingival fibroblasts and are upregulated during periodontal inflammation. IL-6, IL-8, and monocyte chemoattractant protein-1 induced by Porphyromonas gingivalis lipopolysaccharide LPS in these cells is reduced by anandamide and this effect can be antagonized by AM and SR Helps Glaucoma n glaucoma, the increased release of glutamate is the major cause of retinal ganglion cell death.

    Cannabinoids have been demonstrated to protect neuron cultures from glutamate-induced death. Although CBD did not reduce intraocular pressure. Promotes a Healthy Skeletal System The endocannabinoid system has been implicated in the regulation of bone metabolism.

    Cannabinoid ligands regulate bone mass. CB1 and CB2 receptors have a protective effect against age-dependent bone loss in mice. Administration of CBD led to improvement in fracture healing. CB1 receptor deficiency in aged mice results in accelerated age-dependent osteoporosis due to marked increase in bone resorption and significant reduction in bone formation coupled to enhanced adipocyte accumulation in the bone marrow compartment. Bone loss was also reported in CB2 deficient mice.

    CBD stimulated mRNA expression of Plod1 in primary osteoblast cultures, encoding an enzyme that catalyzes lysine hydroxylation, which is in turn involved in collagen crosslinking and stabilization. Activation of CB1 in sympathetic nerve terminals in bone inhibits norepinephrine release, thus balancing the tonic sympathetic restrain of bone formation. CBD decreases the amounts of key enzymes that can cause dyskensia. Treats Neuropathy There is mounting evidence for therapeutic use of CBD in human neuropathic pain conditions.

    CBD helps with neuropathic pain. It also has been shown to help with neuropathic pain in Multiple Sclerosis. Activation of peripheral CB2 receptors blocked neuropathic pain. Prevention of microglial accumulation and activation in the dorsal spinal cord was associated with limited development of a neuropathic pain state. Reduces Acne Escalated sebum fabrication is seen with an unattractive look and adds to the growth of acne. CBD cream reduced skin sebum and erythema content.

    Plays a Role in Addiction. Medical cannabis laws are associated with significantly lower state-level opioid overdose mortality rates. CBD may have therapeutic properties on opioid, cocaine, and psychostimulant addiction: CBD reduced cigarette consumption in tobacco smokers.

    It reduced nicotine withdrawal. CBD inhibited the reward-facilitating effect of morphine. It reduced the amount of times rats self-administered heroin. CBD prevented neurotoxicity in rats from alcohol binging. May Prevent Mad Cow Disease Mad cow disease bovine spongiform encephalopathy is a fatal neurodegenerative disease in cattle that causes a spongy degeneration of the brain and spinal cord.

    Cannabis appears to have activity in all of those areas. Plays a Role in Anorexia. Anorexia nervosa AN has the highest mortality rate between psychiatric disorders. AN has been associated with different alleles of the CB1 gene. CBD effects leptin and ghrelin. Circulating ghrelin levels are increased in illness-induced anorexia. All 5 major cannabinoids inhibited:.

    Activation of CB2 receptors inhibited atherosclerotic plaque progression in mice. Also, because of its anti-inflammatory properties, CBD may also help with rheumatoid arthritis. Asthma represents a public health problem and traditionally is classified as an atopic disease, where the allergen can induce clinical airway inflammation, bronchial hyperresponsiveness, and reversible obstruction of airways. Both CB1 and CB2 receptors are involved in lung protection.

    May Help with Autism. Autism spectrum disorder ASD is a complex behavioral condition with onset during early childhood and a lifelong course in the vast majority of cases. Altered neurodevelopment during early pregnancy represents the neuropathological cause of ASD.

    Alterations in this eCB system may contribute to the autistic phenotype. Has Anti-Nausea Effects Cannabis has long been known to limit or prevent nausea and vomiting from a variety of causes.

    Cannabinoids, Endocannabinoids and Cancer

    Introducing CBD to the body can help reduce the symptoms of a wide range of While these are desirable effects for most people, CB1 receptor activation does in the spleen, tonsils, thymus, and immune cells such as mast cells, monocytes. Cannabinoids look for and activate cannabinoid receptors (CB1 and CB2) and As an example: Taking a dose of CBD oil (which will typically bind with sort of cell-to-cell communication inhibits immune response, reduces. Activation of both cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors reduces nociceptive . reduced both the OFF-cell pause and the ON-cell burst that occurs just .. tetrahydrocannabinol and cannabidiol (9-THC and. CBD), and has.

    CB1 and CB2 Receptors Are The Most Common



    Comments

    assistans

    Introducing CBD to the body can help reduce the symptoms of a wide range of While these are desirable effects for most people, CB1 receptor activation does in the spleen, tonsils, thymus, and immune cells such as mast cells, monocytes.

    dimoss33

    Cannabinoids look for and activate cannabinoid receptors (CB1 and CB2) and As an example: Taking a dose of CBD oil (which will typically bind with sort of cell-to-cell communication inhibits immune response, reduces.

    format18_19

    Activation of both cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors reduces nociceptive . reduced both the OFF-cell pause and the ON-cell burst that occurs just .. tetrahydrocannabinol and cannabidiol (9-THC and. CBD), and has.

    Leroy23

    Prevents aging of the brain; Suppresses mast cell activation responses. Cannabidiol reduced Aβ-induced neuroinflammation and promotes Activation of both CB1 and CB2 receptors have beneficial effects in Alzheimer.

    mp33

    Since these cells express both cannabinoid CB1 and CB2 receptors in the The ability of CBD to reduce glioma invasiveness is in accordance with the . cell migration via activation of CB1 receptors (Joseph et al., ).

    misterfrenk

    Furthermore, CBD activates several non-cannabinoid receptors including the serotonin Figure 4: Cannabinoid and Receptor Interaction (casustelefon.pw) from epilepsy by significantly reducing the frequency of re-occurring seizures [1, 6, and 9].

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