scholarly journals Cannabidiol in dentistry: a scoping review

2020 ◽  
Author(s):  
Carla David ◽  
--- ◽  
Alejandro Elizalde
Keyword(s):  
Scoping Review ◽  
Cannabinoid Receptor ◽  
Oral Diseases ◽  
Scientific Publications ◽  
Cannabinoid Receptor 2 ◽  
Periodontal Tissues ◽  
Positive Therapeutic Effect ◽  
Treatment Action

The CBD has many reports of pharmacological effects in various models of pathologies, ranging from inflammatory and neurodegenerative diseases, epilepsy, autoimmune disorders such as multiple sclerosis, arthritis, schizophrenia among others (1). In other medical areas has been developing CBD as great therapeutic possibilities, with much research in pre-clinical phases (laboratory tests), reviews about complex diseases of the oral cavity (2) and expression of endocannabinoids receptors in the dental and periodontal tissues (3,4). However, the use of CBD in the dental field has been poorly studied and limited, and its effects in the treatment of oral diseases are not well known and reported. Similarly, knowing its properties, mechanisms of action and favorable results in the treatment of other oral diseases, it is believed that it may have a positive therapeutic effect in some pathologies of CBD therapeutic dentistry based on scientific publications that discuss its mechanism of treatment action, suggesting possibilities for future investigations on the use of this compound in dentistry in previous years. Therefore, the purpose of this scoping review will be to map the available evidence to provide an overview and technology of the use of cannabidiol, its effects, and related products in dentistry.References.1.PISANTI, Simona, et al. Cannabidiol: State of the art and new challenges for therapeutic applications. Pharmacology & therapeutics, vol. 175, p. 133-150, 2017. DOI: https://doi.org/10.1016/j.pharmthera.2017.02.041. 2.CUBA, L. F., et al. Cannabidiol: an alternative therapeutic agent for oral mucositis?. Journal of clinical pharmacy and therapeutics, 2017, vol. 42, no 3, p. 245-250.3. Abidi, Ammaar H., et al. "Anti-inflammatory activity of cannabinoid receptor 2 ligands in primary hPDL fibroblasts." Archives of oral biology 87 (2018): 79-85.4.KONERMANN, Anna, et al. In vivo and in vitro identification of endocannabinoid signaling in periodontal tissues and their potential role in local pathophysiology. Cellular and molecular neurobiology, 2017, vol. 37, no 8, p. 1511-1520.

scholarly journals Cannabinoid receptor 2 deletion deteriorates myocardial infarction through the down-regulation of AMPK-mTOR-p70S6K signaling-mediated autophagy

2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Yao Hu ◽  
Yu Tao ◽  
Jing Hu
Keyword(s):  
Myocardial Infarction ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Cannabinoid Receptor ◽  
Cell Counting ◽  
Protective Effects ◽  
Cannabinoid Receptor 2 ◽  
Related Proteins

AbstractCannabinoid receptor 2 (CB2R) has been reported to play an important role in the regulation of pathogenesis and progression of myocardial infarction (MI). Here we tried to investigate its potential mechanisms. The ratio of infarct size in heart issue was detected by TTC staining, and cardiac functions were calculated according to echocardiographic evaluation. Cell viability in cardiomyocytes was investigated by Cell Counting Kit-8 (CCK-8) and lactate dehydrogenase (LDH) release assays. Western blot was used to detect autophagy-related proteins including Beclin-1, LC3, p62, adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK)-mammalian target of rapamycin rabbit (mTOR)-p70 ribosomal protein S6 kinase (p70S6K) signaling-related proteins including AMPK, mTOR, p70S6K, and their phosphorylation formation. Rapamycin was used for the induction of autophagy. Cleaved caspase-3 and Bax were detected for analyzing apoptosis. TEM was used for the detection of autophagosomes. We found that CB2R deletion (CB2R KO) largely deteriorated the severity of MI and the cardiac function as well as cell viability of cardiomyocytes. Knocking out CB2R decreased the level of autophagy in heart issues from MI mice as well as cardiomyocytes under oxygen-glucose deprivation (OGD). Furthermore, CB2R dysfunction significantly attenuated the cardiac protective effects of rapamycin both in vivo and in vitro. Finally, we found that CB2R-mediated autophagy was induced by AMPK-mTOR-p70S6K signaling pathway. Our current study demonstrated for the first time that CB2R deletion led to a detrimental effect of MI through the dysfunction of AMPK-mTOR-p70S6K signaling pathway, which might provide a novel insight in the treatment of MI.

scholarly journals Signaling through cannabinoid receptor 2 suppresses murine dendritic cell migration by inhibiting matrix metalloproteinase 9 expression

Blood ◽  
2012 ◽  
Vol 120 (18) ◽  
pp. 3741-3749 ◽  
Author(s):  
Sabina Adhikary ◽  
Virginia P. Kocieda ◽  
Jui-Hung Yen ◽  
Ronald F. Tuma ◽  
Doina Ganea
Keyword(s):  
Matrix Metalloproteinase ◽  
Cannabinoid Receptor ◽  
Matrix Metalloproteinase 9 ◽  
Cns Injury ◽  
Migration Assay ◽  
Cannabinoid Receptor 2 ◽  
Subsequent Decrease ◽  
Metalloproteinase 9

Abstract Administration of cannabinoid receptor 2 (CB2R) agonists in inflammatory and autoimmune disease and CNS injury models results in significant attenuation of clinical disease, and reduction of inflammatory mediators. Previous studies reported that CB2R signaling also reduces leukocyte migration. Migration of dendritic cells (DCs) to various sites is required for their activation and for the initiation of adaptive immune responses. Here, we report for the first time that CB2R signaling affects DC migration in vitro and in vivo, primarily through the inhibition of matrix metalloproteinase 9 (MMP-9) expression. Reduced MMP-9 production by DCs results in decreased migration to draining lymph nodes in vivo and in vitro in the matrigel migration assay. The effect on Mmp-9 expression is mediated through CB2R, resulting in reduction in cAMP levels, subsequent decrease in ERK activation, and reduced binding of c-Fos and c-Jun to Mmp-9 promoter activator protein 1 sites. We postulate that, by dampening production of MMP-9 and subsequent MMP-9–dependent DC migration, cannabinoids contribute to resolve acute inflammation and to reestablish homeostasis. Selective CB2R agonists might be valuable future therapeutic agents for the treatment of chronic inflammatory conditions by targeting activated immune cells, including DCs.

scholarly journals Activation of cannabinoid receptor 2 alleviates glucocorticoid-induced osteonecrosis of femoral head with osteogenesis and maintenance of blood supply

2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Houyi Sun ◽  
Weicheng Zhang ◽  
Ning Yang ◽  
Yi Xue ◽  
Tianhao Wang ◽  
...  
Keyword(s):  
Femoral Head ◽  
Blood Supply ◽  
Cannabinoid Receptor ◽  
Umbilical Vein ◽  
Tunel Staining ◽  
Tartrate Resistant Acid Phosphatase ◽  
Alizarin Red ◽  
Cannabinoid Receptor 2

AbstractIn glucocorticoid (GC)-induced osteonecrosis of the femoral head (ONFH), downregulated osteogenic ability and damaged blood supply are two key pathogenic mechanisms. Studies suggested that cannabinoid receptor 2 (CB2) is expressed in bone tissue and it plays a positive role in osteogenesis. However, whether CB2 could enhance bone formation and blood supply in GC-induced ONFH remains unknown. In this study, we focused on the effect of CB2 in GC-induced ONFH and possible mechanisms in vitro and in vivo. By using GC-induced ONFH rat model, rat-bone mesenchymal stem cells (BMSCs) and human umbilical vein endothelial cells (HUVECs) to address the interaction of CB2 in vitro and in vivo, we evaluate the osteogenic and angiogenic effect variation and possible mechanisms. Micro-CT, histological staining, angiography, calcein labeling, Alizarin red staining (ARS), alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRAP) staining, TUNEL staining, migration assay, scratch assay, and tube formation were applied in this study. Our results showed that selective activation of CB2 alleviates GC-induced ONFH. The activation of CB2 strengthened the osteogenic activity of BMSCs under the influence of GCs by promotion of GSK-3β/β-catenin signaling pathway. Furthermore, CB2 promoted HUVECs migration and tube-forming capacities. Our findings indicated that CB2 may serve as a rational new treatment strategy against GC-induced ONFH by osteogenesis activation and maintenance of blood supply.

scholarly journals Targeting CYP2J2 to Enhance the Anti-Glioma Efficacy of Cannabinoid Receptor 2 Stimulation by Inhibiting the Pro-Angiogenesis Function of M2 Microglia

2020 ◽  
Vol 10 ◽  
Author(s):  
Xuejiao Lei ◽  
Xuezhu Chen ◽  
Yulian Quan ◽  
Yihao Tao ◽  
Junlong Li
Keyword(s):  
Cellular Proliferation ◽  
Cannabinoid Receptor ◽  
Tube Formation ◽  
Epoxyeicosatrienoic Acid ◽  
Cannabinoid Receptor 2 ◽  
Cancer Management ◽  
Qrt Pcr ◽  
M2 Microglia

Enhancing the therapeutic efficacy of anti-tumor drugs is essential for cancer management. Although cannabinoid receptor 2 (CB2R) stimulation exerts anti-tumor action in glioma cells by regulating cellular proliferation, differentiation, or apoptosis, selective CB2R agonist alone does not achieve a satisfactory therapeutic outcome. Herein, we aimed to evaluate the possible strategy for enhancing the anti-glioma efficacy of JWH133, a selective CB2R agonist. In this study, immunofluorescence and qRT-PCR were used to investigate microglia polarization. Tumor growth was monitored via bioluminescent imaging using the IVIS Spectrum System. The angiogenesis of human brain microvascular endothelial cells (HBMECs) was detected by the tube formation assay. qRT-PCR was used to investigate cytochrome P450 2J2 (CYP2J2) and 11,12-epoxyeicosatrienoic acid (11,12-EET) expression. Our results showed that administration of JWH133 significantly promoted microglial M2 polarization both in vitro and in vivo. The medium supernatant of M2 microglia induced by JWH133 treatment facilitated angiogenesis of HBMECs. CYP2J2 expression and 11,12-EET release in the supernatant of JWH133-induced M2 microglia were significantly upregulated. Treatment with 11,12-EET prompted HBMEC angiogenesis and glioma growth. CYP2J2 knockdown restrained the release of 11,12-EET and significantly enhanced the anti-tumor effect of JWH133 on glioma. This study showed that targeting CYP2J2 might be a beneficial strategy to enhance the anti-glioma efficacy of JWH133 by inhibiting the pro-angiogenesis function of M2 microglia.

Cannabinoid receptor 2 selective agonists stimulate osteoclast formation in vitro but act as anabolic agents in vivo by stimulating bone formation

Bone ◽  
2008 ◽  
Vol 42 ◽  
pp. S31
Author(s):  
Antonia Sophocleous ◽  
Euphemie Landao ◽  
Rob vant Hof ◽  
Aymen I. Idris ◽  
Stuart H. Ralston
Keyword(s):  
Bone Formation ◽  
Cannabinoid Receptor ◽  
Osteoclast Formation ◽  
Anabolic Agents ◽  
Cannabinoid Receptor 2 ◽  
Selective Agonists

The Role of nitro (NO2-), chloro (Cl), and fluoro (F) Substitution in the Design of Antileishmanial and Antichagasic Compounds

2020 ◽  
Vol 21 ◽  
Author(s):  
Boniface Pone ◽  
Ferreira Igne Elizabeth
Keyword(s):  
Chagas Disease ◽  
Mammalian Cells ◽  
Neglected Tropical Diseases ◽  
New Drugs ◽  
Pharmacokinetic Studies ◽  
Scientific Publications ◽  
Antitrypanosomal Activity ◽  
Chemical Groups

: Neglected tropical diseases (NTDs) are responsible for over 500,000 deaths annually and are characterized by multiple disabilities. Leishmaniasis and Chagas disease are among the most severe NTDs, and are caused by the Leishmania sp, and Trypanosoma cruzi, respectively. Glucantime, pentamidine and miltefosine are commonly used to treat leishmaniasis, whereas nifurtimox, benznidazole are current treatments for Chagas disease. However, these treatments are associated with drug resistance, and severe side effects. Hence, the development of synthetic products, especially those containing N02, F, or Cl, which chemical groups are known to improve the biological activity. The present work summarizes the information on the antileishmanial and antitrypanosomal activity of nitro-, chloro-, and fluoro-synthetic derivatives. Scientific publications referring to halogenated derivatives in relation to antileishmanial and antitrypanosomal activities were hand searched in databases such as SciFinder, Wiley, Science Direct, PubMed, ACS, Springer, Scielo, and so on. According to the literature information, more than 90 compounds were predicted as lead molecules with reference to their IC50/EC50 values in in vitro studies. It is worth to mention that only active compounds with known cytotoxic effects against mammalian cells were considered in the present study. The observed activity was attributed to the presence of nitro-, fluoro- and chloro-groups in the compound backbone. All in all, nitro and h0alogenated derivatives are active antileishmanial and antitrypanosomal compounds and can serve as baseline for the development of new drugs against leishmaniasis and Chagas disease. However, efforts on in vitro and in vivo toxicity studies of the active synthetic compounds is still needed. Pharmacokinetic studies, and the mechanism of action of the promising compounds need to be explored. The use of new catalysts and chemical transformation can afford unexplored halogenated compounds with improved antileishmanial and antitrypanosomal activity.

scholarly journals Therapeutic Attributes of Endocannabinoid System against Neuro-Inflammatory Autoimmune Disorders

Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3389
Author(s):  
Ishtiaq Ahmed ◽  
Saif Ur Rehman ◽  
Shiva Shahmohamadnejad ◽  
Muhammad Anjum Zia ◽  
Muhammad Ahmad ◽  
...  
Keyword(s):  
Cannabinoid Receptors ◽  
Cannabinoid Receptor ◽  
Therapeutic Potential ◽  
Endocannabinoid System ◽  
Cell Types ◽  
Autoimmune Disorders ◽  
Specific Receptors ◽  
Different Cell Types

In humans, various sites like cannabinoid receptors (CBR) having a binding affinity with cannabinoids are distributed on the surface of different cell types, where endocannabinoids (ECs) and derivatives of fatty acid can bind. The binding of these substance(s) triggers the activation of specific receptors required for various physiological functions, including pain sensation, memory, and appetite. The ECs and CBR perform multiple functions via the cannabinoid receptor 1 (CB1); cannabinoid receptor 2 (CB2), having a key effect in restraining neurotransmitters and the arrangement of cytokines. The role of cannabinoids in the immune system is illustrated because of their immunosuppressive characteristics. These characteristics include inhibition of leucocyte proliferation, T cells apoptosis, and induction of macrophages along with reduced pro-inflammatory cytokines secretion. The review seeks to discuss the functional relationship between the endocannabinoid system (ECS) and anti-tumor characteristics of cannabinoids in various cancers. The therapeutic potential of cannabinoids for cancer—both in vivo and in vitro clinical trials—has also been highlighted and reported to be effective in mice models in arthritis for the inflammation reduction, neuropathic pain, positive effect in multiple sclerosis and type-1 diabetes mellitus, and found beneficial for treating in various cancers. In human models, such studies are limited; thereby, further research is indispensable in this field to get a conclusive outcome. Therefore, in autoimmune disorders, therapeutic cannabinoids can serve as promising immunosuppressive and anti-fibrotic agents.

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