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      Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis.

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          Abstract

          Current arthritis treatments often have side-effects attributable to active compounds as well as route of administration. Cannabidiol (CBD) attenuates inflammation and pain without side-effects, but CBD is hydrophobic and has poor oral bioavailability. Topical drug application avoids gastrointestinal administration, first pass metabolism, providing more constant plasma levels.

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          Most cited references53

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          Impaired nociception and pain sensation in mice lacking the capsaicin receptor.

          M. J. Caterina, A. Leffler, A. Malmberg … (2000)
          The capsaicin (vanilloid) receptor VR1 is a cation channel expressed by primary sensory neurons of the "pain" pathway. Heterologously expressed VR1 can be activated by vanilloid compounds, protons, or heat (>43 degrees C), but whether this channel contributes to chemical or thermal sensitivity in vivo is not known. Here, we demonstrate that sensory neurons from mice lacking VR1 are severely deficient in their responses to each of these noxious stimuli. VR1-/- mice showed normal responses to noxious mechanical stimuli but exhibited no vanilloid-evoked pain behavior, were impaired in the detection of painful heat, and showed little thermal hypersensitivity in the setting of inflammation. Thus, VR1 is essential for selective modalities of pain sensation and for tissue injury-induced thermal hyperalgesia.
          Article 0 comments Cited 568 times – based on 0 reviews     Review now
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            The orphan receptor GPR55 is a novel cannabinoid receptor.

            E Ryberg, N. Larsson, S Sjögren … (2007)
            The endocannabinoid system functions through two well characterized receptor systems, the CB1 and CB2 receptors. Work by a number of groups in recent years has provided evidence that the system is more complicated and additional receptor types should exist to explain ligand activity in a number of physiological processes. Cells transfected with the human cDNA for GPR55 were tested for their ability to bind and to mediate GTPgammaS binding by cannabinoid ligands. Using an antibody and peptide blocking approach, the nature of the G-protein coupling was determined and further demonstrated by measuring activity of downstream signalling pathways. We demonstrate that GPR55 binds to and is activated by the cannabinoid ligand CP55940. In addition endocannabinoids including anandamide and virodhamine activate GTPgammaS binding via GPR55 with nM potencies. Ligands such as cannabidiol and abnormal cannabidiol which exhibit no CB1 or CB2 activity and are believed to function at a novel cannabinoid receptor, also showed activity at GPR55. GPR55 couples to Galpha13 and can mediate activation of rhoA, cdc42 and rac1. These data suggest that GPR55 is a novel cannabinoid receptor, and its ligand profile with respect to CB1 and CB2 described here will permit delineation of its physiological function(s).
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              Rheumatoid arthritis progression mediated by activated synovial fibroblasts.

              Stephanie Lefèvre, Birgit Zimmermann, Steffen Gay … (2010)
              Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovial hyperplasia and progressive joint destruction. Rheumatoid arthritis synovial fibroblasts (RASFs) are leading cells in joint erosion and contribute actively to inflammation. RASFs show an activated phenotype that is independent of the inflammatory environment and requires the combination of several factors. Although new aspects regarding RASF activation via matrix degradation products, epigenetic modifications, inflammatory factors, Toll-like receptor (TLR) activation and others have recently been uncovered, the primary pathophysiological processes in early arthritis leading to permanent activation are mostly unknown. Here, we review new findings regarding RASF activation and their altered behavior that contribute to matrix destruction and inflammation as well as their potential to spread RA. Copyright © 2010 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Eur J Pain
                Title: European journal of pain (London, England)
                Publisher: Wiley
                ISSN (Electronic): 1532-2149
                ISSN (Print): 1090-3801
                Publication date (Electronic): July 2016
                Volume: 20
                Issue: 6
                Affiliations
                [1 ] Department of Pharmaceutical Sciences, University of Kentucky College of Pharmacy, Lexington, KY, 40536-0082, USA.
                [2 ] Department of Physiology, University of Kentucky College of Medicine, Lexington, KY, 40536-0298, USA.
                Article
                Mid ID: NIHMS737474
                DOI: 10.1002/ejp.818
                PMC ID: 4851925
                PubMed ID: 26517407
                SO-VID: e2fd12a4-e220-40d9-ac13-c021eee0a14a
                Copyright © © 2015 European Pain Federation - EFIC®
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