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What shown CBD studies Psoriasis: have for the

fit9
09.06.2018

Content:

  • What shown CBD studies Psoriasis: have for the
  • Cannabinoids as novel anti-inflammatory drugs
  • What is psoriasis?
  • Studies have shown that cannabinoids can help in the treatment efforts of psoriasis by regulating the immune system and managing overactive. The underlying mechanism of psoriasis involves the immune system. As research recently found, the endocannabinoid system constantly binds. A study found that some of the In people with psoriasis, skin cells reproduce In , a study found that the cannabinoids delta tetrahydrocannabinol, cannabidiol.

    What shown CBD studies Psoriasis: have for the

    Both pro-inflammatory and anti-inflammatory effects of THC were demonstrated in this study, proposing that different cell populations have varied thresholds of response to cannabinoids. Interestingly, while the anti-inflammatory cytokine IL decreased following THC treatment, there was an increase in the proinflammatory cytokine IL In other studies, cannabinoid CP55, at nanomolar concentrations was shown to have a stimulatory effect on several cytokines in the human promyelocytic cell line HL [ 27 ].

    In a different study, mice were challenged with Corynebacterium parvum, in vivo , following the administration of the synthetic cannabinoids WIN55, and HU The animals were then challenged with LPS. This effect was shown to be CB1 receptor dependent. During chronic inflammation, IL-6 suppression can decrease tissue injury [ 30 ]. AjA has been reported to prevent joint-tissue injury in animal models of adjuvant arthritis [ 31 ].

    Recent studies showed that addition of AjA to human monocyte-derived macrophages in vitro reduced the secretion of IL-6 from activated cells, suggesting that AjA may have a value for treatment of joint inflammation in patients with systemic lupus erythematosus SLE , rheumatoid arthritis RA and osteoarthritis [ 32 ].

    Recent in vitro studies have also shown the potent anti-inflammatory effect of synthetic cannabinoids CP55, and WIN55, Endocannabinoids have also been reported to affect the cytokine biology of various cell systems. Antiproliferative effects of endocannabinoids on cancer cell lines are well established and are discussed in the later section of the review.

    However, AEA has also been reported to increase cytokine-induced proliferation. Mouse bone marrow cells, when cultured in the presence of IL-3 and AEA, were observed to produce more hematopoietic colonies than with IL-3 alone [ 35 ]. Furthermore, in undifferentiated and macrophage-like differentiated HL cells, 2-AG induced CB2-dependent acceleration in the production of IL-8 [ 37 ]. On a contrary note, cytokines have also been shown to affect the endocannabinoid system.

    Table 2 provides a summary of the effect of cannabinoids on cytokines and chemokines in various cell models [ 26 , 28 , 29 , 32 — 34 , 37 , 40 , 41 ].

    CXC-chemokine ligand 8; ND: The action of these cells leads to the demyelination of nerve fibers and axons in the CNS of humans and results in many signs and symptoms, such as muscle spasms, tremor, ataxia, weakness or paralysis, constipation and loss of bladder control [ 42 ].

    There is both anecdotal and clinical evidence to show the effectiveness of cannabinoids in the treatment of MS. In , a survey of MS patients 57 men and 55 women from the USA and UK was conducted; all of the patients were self-medicating with a form of cannabis.

    Use of cannabinoids also improved objective test results such as hand-writing tests and bladder control tests [ 43 , 44 ]. In general, cannabinoids are useful in treating MS because they have neuroprotective as well as immunosuppressive properties [ 44 , 45 ]. In this section, we will focus on the latter and discuss the action of endogenous, natural and synthetic cannabinoids on immune cells within the CNS during MS.

    The destruction of the blood—brain barrier in MS is initiated by myelin-specific self-reactive T cells. Infiltration of these cells into the spinal cord and CNS, and their subsequent activation, leads to the elimination of the myelin sheath around the nerves and axons [ 46 , 47 ].

    More recently, Th17 cells have been shown to be involved in the pathogenesis of MS [ 48 , 49 ]. One mechanism of immunosuppression by cannabinoids is the induction of apoptosis and Sanchez et al.

    A CB1-mediated suppressive pathway has also been shown in myelin-specific T cells [ 24 ]. Microglial cells are the macrophages of the CNS and, during MS, they mediate tissue injury in two main ways: In the initial stages of inflammation, after activation, microglial cells present antigens to myelin-specific T cells, which results in the activation and proliferation of Th1 lineage cells.

    The investigators confirmed this finding by studying the morphology of the cells reactive vs resting as well as by immunohistochemistry. In the later stages of disease, microglial cells secrete IL, IL and IL, nitric oxide and glutamate and contribute to myelin sheath destruction. IL drives the proliferation of Th1 cells while IL is important in the maintenance of Th17 cells.

    A recent study by Correa et al. Cannabinoids also exert their immunosuppressive effects on astrocytes. During disease progression, astrocytes are activated to secrete cytokines, chemokines and nitric oxide, thereby contributing to the overall inflammatory response.

    Because astrocytes express both CB1 and CB2 receptors, several studies investigated the inhibitory role of cannabinoids on this cell population in the context of MS. The precise role of IL-6 in the CNS is still unclear; however, it has been reported that IL-6 secretion potentiates neuronal growth factor production.

    In , Sheng et al. The three main cell types that are involved in demyelination of the nerve fibers and axons in the CNS include activated T-cells, microglia and astrocytes. In activated T-cells, treatment with WIN 55,, AEA and JWH has been shown to inhibit cytokine production, infiltration of cells into the spinal cord and in vitro recall response to myelin oligodendrocyte glycoprotein by T-cells. Cannabinoids also inhibit the antigen presenting abilities of microglia by downregulating MHCII expression, costimulatory molecule CD40 expression, as well as cytokine secretion.

    Astrocytes, the major cell population in the brain, are also affected, as cannabinoid binding to the receptors leads to inhibition of inflammatory molecules, such as nitric oxide, cytokines and chemokines. In addition, anandamide binding leads to secretion of neural growth factor secretion and protection of the neurons in the CNS.

    During inflammation, several different cellular pathways are activated in the intestinal tract, leading to a pathological state [ 58 ]. Functional CB1 receptor has been shown to be expressed in the human ileum and colon and the number of CB1-expressing cells was found to be significantly increased after inflammation [ 59 , 60 ].

    A protective role for these CB1 receptors during inflammation has been shown in a study analyzing the role of the endogenous cannabinoid system in the development of experimental colitis in mice, induced by intrarectal 2,4-dinitrobenzene sulfonic acid DNBS treatment or oral dextran sodium sulfate DSS administration [ 59 ].

    The DSS model, originally reported by Okayasu et al. Furthermore, long-term DSS administration produces colorectal carcinoma, which is similar to the dysplasia—carcinoma sequence seen in the course of cancer development in human ulcerative colitis [ 62 ]. The involvement of the endogenous cannabinoid system in the modulation of the acute phase of DNBS-induced colitis was further supported by the increased levels of transcripts coding for CB1 in wild-type mice after induction of inflammation.

    It was observed that genetic ablation of CB1 receptors rendered mice more sensitive to inflammatory insults. Furthermore, similar to results observed in CB1-deficient mice, pharmacological blockade of CB1 with the specific antagonist SRA led to a worsening of colitis [ 59 ]. The protective role of the endogenous cannabinoid system was observed 24 h after DNBS treatment and became more evident on days 2 and 3. This gives further support to the notion that the endogenous cannabinoid system is protective against inflammatory changes.

    These data indicated that the activation of CB1 and the endogenous cannabinoid system is an early and important physiological step in self-protection of the colon against inflammation. Pharmacological stimulation of cannabinoid receptors with the potent agonist HU also induced a reduction of experimental colitis. It has been reported that cannabinoid receptor stimulation could have a beneficial effect on experimental colitis [ 64 ].

    Intraperitoneal application of ACEA, a CB1-selective agonist, and JWH, a CB2-selective agonist, inhibited oil of mustard OM -induced colitis and subsequent symptoms such as induced distal colon weight gain, colon shrinkage, inflammatory damage, diarrhea and histological damage. This study demonstrated a role for CB2 activation in experimental colitis. The fact that both CB1 and CB2 agonists are active in colitis models lends additional support to the theory that signaling through cannabinoid receptors may mediate protective mechanisms in colitis.

    In the small intestine, the involvement of CB1 receptors in the control of intestinal motility during croton oil-induced inflammation was recently demonstrated. It was further suggested that increased levels of CB1 receptor expression in inflamed jejuna may contribute to this protective effect. CB1 receptors were shown to modulate gastrointestinal motility during croton oil-induced inflammation in mice. Fatty acid amide hydrolase is the major enzyme involved in the degradation of several bioactive fatty amides, in particular anandamide [ 11 ], and its genetic deletion in mice leads to a strongly decreased ability to degrade this endocannabinoid and an increase of anandamide levels in several tissues [ 66 ].

    In conclusion, cannabinoids have been shown to regulate the tissue response to excessive inflammation in the colon, mediated by both dampening smooth-muscular irritation caused by inflammation and suppressing proinflammatory cytokines, thus controlling the cellular pathways leading to inflammatory responses.

    These results strongly suggest that modulation of the physiological activity of the cannabinoid system during colonic inflammation might be a promising therapeutic tool for the treatment of several diseases characterized by inflammation of the GI tract. During the past few years, awareness of the cannabinoid system in the pathophysiology of liver disease has gained momentum.

    Both CB1 and CB2 receptors have been shown to be upregulated in the early stages of liver injury [ 68 — 72 ]. Although embryonic liver has been shown to express CB2 receptor mRNA, adult liver hepatocytes and endothelial cells displayed only a faint physiological level of expression of CB1 receptors and were shown to produce low levels of endocannabinoids.

    CB1 receptors have been found to be upregulated in the vascular endothelium and in myofibroblasts located in fibrotic bands of cirrhotic livers in human and rodents [ 72 ]. CB2 receptors are also expressed in myofibroblasts, inflammatory cells and biliary epithelial cells [ 69 ]. There has been growing evidence in recent years to suggest that endocannabinoids may regulate the pathophysiology of liver diseases, including both acute forms of hepatic injury, liver fibrosis and cirrhosis.

    The endocannabinoids are found in low levels in normal liver, which may be due to high levels of expression of FAAH, which is responsible for the breakdown of AEA [ 11 ]. The levels of AEA have been shown to increase in the liver and serum during acute hepatitis and fatty liver disease [ 70 ].

    Together, the above studies suggest that endocannabinoids and their receptors may play a critical role in regulating liver fibrogenesis; therefore, targeting the cannabinoid receptors may serve as a novel tool to prevent and treat liver injury.

    While the mechanisms of inflammatory liver injury are unclear, they are accompanied by infiltration of activated polymorphonuclear leukocytes, activation of Kupffer cells, production of proinflammatory cytokines and generation of ROS. Many recent studies indicated strongly the increased upregulation of the endocannabinoid system during liver diseases involving hepatocyte injury, inflammation, fibrogenesis, hepatic encephalopathy, cirrhotic cardiomyopathy and portal hypertension [ 73 ].

    Moreover, pretreatment of mice with JWH, a CB2 receptor agonist, was shown to decrease the degree of liver tissue injury and inflammatory cell infiltration and decrease serum levels of cytokines, chemokines and adhesion molecules [ 74 ]. The data also highlights the protective role of CB2 receptor activation in the inflammatory response associated with chronic liver diseases such as viral hepatitis and alcoholic or nonalcoholic fatty liver diseases.

    Viral hepatitis, alcohol abuse and nonalcoholic fatty liver are some of the conditions that can induce chronic liver injury and inflammation, leading to activation of fibrogenesis as a wound-healing mechanism. However, persistence of fibrogenic stimuli can enhance deposition of the extracellular matrix by hepatic myofibroblasts, thus disrupting normal liver architecture and, ultimately, leading to cirrhosis and liver failure.

    CB1 and CB2 receptors are shown to be markedly upregulated in cirrhotic human liver samples, demonstrating the impact of endocannabinoids in liver fibrogenesis. In addition, increases in circulating levels of anadamide and hepatic 2-AG have also been reported in cirrhosis and liver fibrosis, respectively [ 73 ].

    By contrast, activation of CB1 receptors was found to promote profibrotic response [ 72 ]. Further effects of the endocannabinoids have also been shown to be receptor independent. AEA and 2-AG have been shown to induce necrosis and apoptosis, respectively, in activated hepatic stellate cells, through increased generation of ROS [ 76 ]. The abuse of cannabis has been shown to promote liver fibrosis in patients with chronic hepatitis C, indicating that cannabinoids may exacerbate liver fibrogenesis and that CB1 receptor antagonists may play a role as anti-fibrosing molecules [ 71 ].

    However, an alternative explanation could be that marijuana can trigger immunosuppression. For example, CB2 activation in immune cells can trigger apoptosis and this, in turn, can have an immunosuppressive effect in patients with hepatitis C.

    As such patients require immunocompetent cells to keep hepatitis under control, chronic marijuana abuse may promote fibrogenesis through the activation of CB2 and consequent suppression of antiviral immunity [ 77 ]. Endocannabinoids may also regulate liver cirrhosis by acting as mediators of vascular and cardiac functions.

    Endocannabinoids can trigger vasorelaxation, while an upregulated CB1-mediated cannabinoid tone causes enhanced mesenteric vasodialation leading to portal hypertension [ 73 , 75 ]. A recent in vivo study by Batkai et al. Further improvement in contractile function of isolated papillary muscles was observed following treatment with AM, a CB1 receptor antagonist, suggesting therapeutic potential against cirrhotic cardiomyopathy [ 75 ].

    There are limited, but reliable, data on the neuroprotective role of the endocannabinoid system in hepatic encephalopathy.

    It has been demonstrated in a murine model that, during fulminant hepatic failure, levels of 2-AG in the brain are elevated, potentially as a response to liver damage. Thus, influencing the endocannabinoid system with exogenous cannabinoid derivates specific for the CB1 or CB2 receptor may have a beneficial therapeutic effect on neurological dysfunction in liver diseases [ 78 ]. Recently, we noted that both exogenous and endogenous cannabinoids protected mice from concanavalin-A ConA -induced acute hepatitis, a model that mimics viral or autoimmune hepatitis, in which T cells play a critical role in triggering liver injury.

    We found that administration of a single dose of THC or anandamide could ameliorate Con-A-induced hepatitis. This overwhelming evidence shows that the cannabinoid system must play a major role in the pathophysiology of various liver diseases and its therapeutic potential should be exploited for the treatment of chronic liver injuries Figure 2. Endocannabinoids, CB1 antagonists and CB2 agonists as potential drugs for the treatment of liver injury.

    The major immune cell populations involved in joint injury are macrophages, T cells, fibroblast-like synoviocytes and DCs. Cannabinoids and their anti-inflammatory properties have been studied in animal models of RA and on human cells from RA patients and these studies demonstrate the anti-arthritic properties of these natural plant compounds [ 32 , 82 — 84 ].

    Interestingly, most of the studies on RA and cannabinoids focus on the use of nonpsychoactive cannabinoids. CBD is the major nonpsychoactive component of the cannabis plant and its protective effect has been shown in murine collagen-induced arthritis [ 85 ]. Lymph node cells from HUtreated mice showed decreased proliferative responses when the cells from 7-day post-inflammation mice were incubated with collagen II.

    In a different study, Parker et al. AjA also exerts its immunomodulatory effects by inducing apoptosis in mature osteoclast-like cells and, therefore, protecting the host from osteoclastogenesis. The hallmarks of cancer-related inflammation include the presence of inflammatory cells in tumor tissue, and the regulation of tumor growth, metastasis and angiogenesis by inflammatory mediators e. The connection between inflammation and cancer is now generally accepted and nonsteroidal anti-inflammatory drugs have been shown to reduce varied cancer risk.

    Hence, inflammation can be considered as a therapeutic opportunity in certain types of cancer. Recent applications of cannabinoids have been extended as antitumor agents [ 1 , 88 ], which relies on their ability to inhibit tumor angiogenesis [ 89 ] or induce direct apoptosis or cell cycle arrest in neoplastic cells [ 89 — 92 ]. A focus on the antiproliferative effects of these compounds in various tumors, such as breast and prostate cancers, pheochromocytoma and malignant gliomas, has been proposed [ 1 , 92 — 94 ].

    Our laboratory reported that, in vitro , THC and other cannabinoids could induce apoptosis in transformed murine and human T cells [ 95 ], including primary acute lymphoblastic human leukemia cells. The role of endocannabinoids as potential endogenous tumor growth inhibitors has been suggested in a study where it was observed that levels of both AEA and 2-AG were higher in precancerous polyps than in fully developed carcinomas in the colon [ 98 ]. Recent in vivo studies proposed that selective targeting of CB2 receptors resulted in colorectal tumor growth inhibition via apoptosis, which was mediated through the stimulation of ceramide [ 98 ].

    In a xenograft model of thyroid cancer, substances that blocked endocannabinoid degradation also increased the levels of AEA and 2-AG in the tissue and reduced tumor growth [ 99 ]. Various attempts have been made to inactivate cannabinoid-degrading enzymes, thereby increasing the local concentration of endocannabinoids at the tumor cell surface. This leads to anti-tumor effects of CB receptor signaling in various cancer types, such as thyroid, brain and prostate cancer [ 99 — ].

    Although the majority of the effects of cannabinoids are CB receptor mediated, AEA has been shown to induce its effects on cancerous cells by interacting with TRPV1 receptor [ , ] or cholesterol-rich lipid rafts [ ].

    Furthermore, it has been reported that signaling pathways are differentially regulated by cannabinoids in normal cells versus cancer cells. In malignancies, such as thyroid cancer, lymphoma, melanoma, pancreas and breast cancer, the levels of cannabinoid receptors are often higher in the tumor compared with normal cells of the same origin, resulting in increased sensitivity to cannabinoids in the malignancies [ 89 , — ].

    Moreover, many animal studies have reported antiproliferative and pro-apoptotic effects of cannabinoids on tumor cells but not on normal tissue [ 89 , 91 ]. Thus, the role of the cannabinoid system in cancer indicates that this system is involved in regulating many of the functions that are essential in cancer development.

    Allergic asthma is a complex inflammatory disorder characterized by airway hyper-responsiveness, elevated serum IgE, recruitment of eosinophils into the lung and mucus hypersecretion by goblet cells [ ]. While most studies have shown that cannabinoids, such as THC, facilitate a Th1 to Th2 cytokine switch, as discussed previously, it is surprising that cannabinoids can also suppress allergic asthma triggered primarily by Th2 cytokines. Previous findings indicated that aerosolized THC was capable of causing significant bronchodilatation with minimal systemic side effects, but had a local irritating effect on the airways [ ].

    Further bronchodilator effects of cannabinoids administered orally or by aerosol to asthmatic patients have also been reported [ , ]. Similarly, endogenous cannabinoids have been shown to regulate airway responsiveness. It was reported that activation of CB1 receptors by locally released anandamide may participate in the control of bronchial contractility. However, the authors further suggested that the effects of AEA may depend on the state of the bronchial muscle.

    During capsaicin-evoked bronchospasm, AEA may reduce the muscle contraction, whereas AEA may cause bronchoconstriction in the absence of vagus nerve-constricting tone [ ].

    Cannabidiol has been shown to be effective in protecting endothelial function and integrity in human coronary artery endothelial cells HCAECs. In addition, proliferation and migration was markedly increased in activated cell populations. The use of CB2 agonists JWH and HU inhibited all activated pathways in a dose-dependent manner, establishing a novel use for these cannabinoid compounds [ ]. EAU was strongly inhibited when the CB2 was engaged and the effects of CB2 engagement appeared to be mediated predominantly through downregulation of T-cell function with a less-marked effect on antigen presentation [ ].

    An impaired T-cell-proliferative response in leukocytes from JWHtreated mice was also accompanied by marked reductions in cytokine production. A study performed by Li et al.

    Similarly, CBD treatment has been shown to significantly inhibit and delay destructive insulitis and inflammatory Th1-associated cytokine production in nonobese diabetes-prone NOD female mice. A recent study indicated that treatment of 11—week-old female NOD mice, either in a latent diabetes stage after 14 weeks or with initial symptoms of diabetes appearing up to 14 weeks with CBD for 4 weeks, could lead to sustained inhibition of insulitis [ ].

    CBD treatment inhibited specific destruction of the islets and reduced the infiltrates by mononuclear cells into the islets, thus preventing diabetes.

    Furthermore, cannabinoids have also been demonstrated to possess additional beneficial effects in animal models of diabetes. It has been reported that rats treated with CBD for periods of 1—4 weeks experienced significant protection from diabetic retinopathy [ ].

    Cannabinoids have also been shown to alleviate neuropathic pain associated with the disease. Mice injected with a cannabis receptor agonist experienced a reduction in diabetic-related tactile allodynia compared with nontreated controls [ ]. Thus, cannabinoids can be considered useful for controlling T1D due to their anti-inflammatory properties.

    It is becoming increasingly clear that cannabinoid receptors and their endogenous ligands play a crucial role in the regulation of the immune system.

    Exogenous cannabinoids have been shown to suppress T-cell-mediated immune responses by primarily inducing apoptosis and suppressing inflammatory cytokines and chemokines. Such observations indicate that targeting cannabinoid receptor—ligand interactions may constitute a novel window of opportunity to treat inflammatory and autoimmune disorders. As CB2 receptors are primarily expressed on immune cells, targeting CB2 may result in selective immunomodulation without overt toxicity.

    The future challenges for the use of cannabinoids as anti-inflammatory drugs include synthesis of cannabinoid receptor agonists that are nonpsychoactive with anti-inflammatory activity and then identifying their mode of action.

    Although current studies suggest that cannabinoids are useful therapeutic agents in the treatment of various inflammatory disorders, further evaluation of the mechanisms that account for their anti-inflammatory properties is necessary. Such studies may involve the use of cannabinoid receptor-knockout mice and use of receptor-specific compounds. Whether endocannabinoids and cannabinoid receptors play a critical role during normal inflammatory response also requires further consideration.

    Moreover, cannabinoid receptor signaling and effect of cannabinoids on adhesion molecules, co-stimulatory molecules and chemokines require further study in order to increase our understanding of cannabinoids and their intricate effects on immune system disorders.

    Overall, cannabinoids have exhibited significant potential to be used as novel anti-inflammatory agents and specific targeting of CB2 receptors holds the promise of mediating immunosuppressive effects without exerting psychotropic side effects. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript.

    This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties. For reprint orders, please contact moc. No writing assistance was utilized in the production of this manuscript.

    National Center for Biotechnology Information , U. Author manuscript; available in PMC Aug 1. Author information Copyright and License information Disclaimer. The publisher's final edited version of this article is available at Future Med Chem. See other articles in PMC that cite the published article. Abstract Cannabinoids are a group of compounds that mediate their effects through cannabinoid receptors.

    Table 1 Selected cannabinoid molecules. Open in a separate window. Infections, stress, dry skin and certain medicines can make symptoms worse. Psoriasis is likely caused by a type of white blood cells that mistakenly attack healthy skin cells.

    These overactive T cells also trigger additional immune responses, causing blood vessels in the skin to dilate. Genetics may play a role, but environmental factors such as infections, skin injuries, stress, cold weather, smoking, heavy alcohol consumption and certain medications may trigger psoriasis.

    Psoriasis may also cause swollen and stiff joints and thickened or ridged nails in a condition called psoriatic arthritis.

    Joints throughout the entire body can be affected, including the spine and fingers. The signs and symptoms can resemble those of rheumatoid arthritis. The condition can also cause pain in the feet and lower back, and swollen fingers and toes.

    While psoriasis cannot be cured, certain treatments can slow how quickly skin cells grow and offer relief. Medications such as topical corticosteroids, vitamin D analogues, anthralin, topical retinoids, calcineurin inhibitors and salicylic acid can help manage inflammation, reduce scaling and encourage dead skin cell sloughing. Additionally, moisturizers and sunlight exposure can also help improve psoriasis symptoms. Studies indicate that the cannabinoids found within cannabis can help manage psoriasis through their interaction with the endocannabinoid system.

    When the endocannabinoid system is disrupted, it can lead to the development of autoimmune diseases like psoriasis. Earlier clinical trial data found that cannabis helps prevent psoriasis flare-ups by activating the cannabinoid 2 CB 2 receptors of the ECS 4.

    Research also suggests that cannabis can help treat psoriasis symptoms by managing the over activity of T cells. Four of the major cannabinoids found within cannabis, including tetrahydrocannabinol THC , cannabidiol CBD , cannabinol CBN and cannabigerol CBG , have been shown to effectively inhibit overactive T cells and thereby play a therapeutic role in psoriasis treatment efforts Additionally, studies have found that through the activation of CB2 receptors, cannabinoids can help alleviate, and in some cases reverse, skin inflammation damage 6.

    With the recent passing of HB , the state will allow minors under 18 with psoriasis to use medical cannabis starting in October Cannabis for refractory psoriasis-high hopes for a novel treatment and a literature review. Pharmacological properties and therapeutic possibilities for drugs acting upon endocannabinoid receptors. Your email address will not be published. Federal Tax ID The information contained in this website is for general information and educational purposes only.

    It does not constitute medical advice. Therefore, any reliance you place on such information is strictly at your own risk. Please check with your medical doctor before starting or changing your CBD routine.

    Cannabinoids as novel anti-inflammatory drugs

    Has anyone used CBD oil to help their P. If so where from and did you get is advertised in UK as CBD oil or cannabis oil (or what shows up in an What seems recurrent in the research I have done is that food and your. CBD oil for psoriasis has been increasingly emerging as a potentially viable treatment “Research has shown that cannabinoids like CBD can inhibit skin. A study published in the Journal of Dermatological Science in February found that CBD may offer therapeutic value for psoriasis by.

    What is psoriasis?



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