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      Analgesic effect of S (+)‐flurbiprofen plaster in a rat model of knee arthritis: analysis of gait and synovial fluid prostaglandin E 2 levels

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          Abstract

          Objectives

          We developed S (+)‐flurbiprofen plaster ( SFPP), a novel NSAID patch containing S (+)‐flurbiprofen ( SFP), a potent cyclooxygenase ( COX) inhibitor. The purpose of this study was to assess efficacy of SFPP by analysing its effect on the gait disturbance and measuring the prostaglandin E 2 ( PGE 2) production in synovial fluid in a rat model of knee arthritis.

          Methods

          Knee inflammation was induced in rats by intra‐articular injection of a yeast suspension. Subsequently, an NSAID patch containing SFP, ketoprofen or loxoprofen was applied over the affected knee. Gait was assessed at 2, 4 and 6 h after application of the patch. The PGE 2 concentration in the synovial fluid was measured after the gait assessment.

          Key findings

          Application of SFPP (0.125, 0.25, 0.5 or 1 mg/sheet) was followed by a decrease in the visual gait score at all the doses examined. In the case of the other two NSAID patches, only the ketoprofen patch (1 or 2 mg/sheet) and loxoprofen patch (5 mg/sheet) produced a decrease in the visual gait score. All of the NSAID patches decreased the PGE 2 production in the synovial fluid.

          Conclusions

          These results suggest the potential usefulness of SFPP as an analgesic patch in patients with inflammatory joint pain.

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          Most cited references18

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          Prostanoid receptors: structures, properties, and functions.

          Shuh Narumiya, Yukihiko Sugimoto, Fumitaka Ushikubi (1999)
          Prostanoids are the cyclooxygenase metabolites of arachidonic acid and include prostaglandin (PG) D(2), PGE(2), PGF(2alpha), PGI(2), and thromboxne A(2). They are synthesized and released upon cell stimulation and act on cells in the vicinity of their synthesis to exert their actions. Receptors mediating the actions of prostanoids were recently identified and cloned. They are G protein-coupled receptors with seven transmembrane domains. There are eight types and subtypes of prostanoid receptors that are encoded by different genes but as a whole constitute a subfamily in the superfamily of the rhodopsin-type receptors. Each of the receptors was expressed in cultured cells, and its ligand-binding properties and signal transduction pathways were characterized. Moreover, domains and amino acid residues conferring the specificities of ligand binding and signal transduction are being clarified. Information also is accumulating as to the distribution of these receptors in the body. It is also becoming clear for some types of receptors how expression of their genes is regulated. Furthermore, the gene for each of the eight types of prostanoid receptor has been disrupted, and mice deficient in each type of receptor are being examined to identify and assess the roles played by each receptor under various physiological and pathophysiological conditions. In this article, we summarize these findings and attempt to give an overview of the current status of research on the prostanoid receptors.
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            Prostaglandin E2 and pain--an update.

            Atsufumi Kawabata (2010)
            Prostaglandin E(2) (PGE(2)), a cyclooxygenase (COX) product, is the best known lipid mediator that contributes to inflammatory pain. Nonsteroidal anti-inflammatory drugs (NSAIDs), inhibitors of COX-1 and/or COX-2, suppress inflammatory pain by reducing generation of prostanoids, mainly PGE(2), while they exhibit gastrointestinal, renal and cardiovascular toxicities. Selective inhibitors of microsomal PGE synthase-1 and subtype-selective antagonists of PGE(2) receptors, particularly EP(1) and EP(4), may be useful as analgesics with minimized side-effects. Protein kinase C (PKC) and PKA downstream of EP(1) and EP(4), respectively, sensitize/activate multiple molecules including transient receptor potential vanilloid-1 (TRPV1) channels, purinergic P2X3 receptors, and voltage-gated calcium or sodium channels in nociceptors, leading to hyperalgesia. PGE(2) is also implicated in neuropathic and visceral pain and in migraine. Thus, PGE(2) has a great impact on pain signals, and pharmacological intervention in upstream and downstream signals of PGE(2) may serve as novel therapeutic strategies for the treatment of intractable pain.
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              Topical NSAIDs for chronic musculoskeletal pain: systematic review and meta-analysis

              Lorna Mason, R Moore, Jayne E Edwards … (2004)
              A previous systematic review reported that topical NSAIDs were effective in relieving pain in chronic conditions like osteoarthritis and tendinitis. More trials, a better understanding of trial quality and bias, and a reclassification of certain drugs necessitate a new review. Studies were identified by searching electronic databases, and writing to manufacturers. We identified randomised, double blind trials comparing topical NSAID with either placebo or another active treatment, in adults with chronic pain. The primary outcome was a reduction in pain of approximately 50% at two weeks, and secondary outcomes were local and systemic adverse events and adverse event-related withdrawals. Relative benefit and number-needed-to-treat (NNT), and relative harm and number-needed-to-harm (NNH) were calculated, and the effects of trial quality, validity and size, outcome reported, and condition treated, were examined by sensitivity analyses. Twelve new trials were added to 13 trials from a previous review. Fourteen double blind placebo-controlled trials had information from almost 1,500 patients. Topical NSAID was significantly better than placebo with relative benefit 1.9 (95% confidence interval 1.7 to 2.2), NNT 4.6 (95% confidence interval 3.8 to 5.9). Results were not affected by trial quality, validity or size, outcome reported, or condition treated. Three trials with 764 patients comparing a topical with an oral NSAID found no difference in efficacy. Local adverse events (6%), systemic adverse events (3%), or the numbers withdrawing due to an adverse event were the same for topical NSAID and placebo. Topical NSAIDs were effective and safe in treating chronic musculoskeletal conditions for two weeks. Larger and longer trials are necessary to fully elucidate the place of topical NSAIDs in clinical practice.
              Article 0 comments Cited 38 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Ayaka Fukumoto:
                ORCID: http://orcid.org/0000-0002-8407-7018
                a-kaku@taisho.co.jp
                Journal
                Journal ID (nlm-ta): J Pharm Pharmacol
                Journal ID (iso-abbrev): J. Pharm. Pharmacol
                Journal ID (doi): 10.1111/(ISSN)2042-7158
                Journal ID (publisher-id): JPHP
                Title: The Journal of Pharmacy and Pharmacology
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0022-3573
                ISSN (Electronic): 2042-7158
                Publication date (Electronic): 01 April 2018
                Publication date (Print): July 2018
                Volume: 70
                Issue: 7 ( doiID: 10.1111/jphp.2018.70.issue-7 )
                Pages: 929-936
                Affiliations
                [ 1 ] Pharmacology Laboratories Taisho Pharmaceutical Co., Ltd. Saitama Japan
                [ 2 ] Pharmaceutical Business Strategic Planning Taisho Pharmaceutical Co., Ltd. Tokyo Japan
                [ 3 ] Institute for Integrated Sports Medicine Keio University School of Medicine Tokyo Japan
                Author notes
                [*] [* ] Correspondence

                Ayaka Fukumoto, Pharmacology 4, Pharmacology Laboratories Taisho Pharmaceutical Co., Ltd., 1‐403 Yoshino‐cho, Kita‐ku, Saitama‐shi, Saitama 331‐9530, Japan.

                E‐mail: a-kaku@ 123456taisho.co.jp

                Author information
                http://orcid.org/0000-0002-8407-7018
                Article
                Publisher ID: JPHP12914
                DOI: 10.1111/jphp.12914
                PMC ID: 6033094
                PubMed ID: 29607510
                SO-VID: e957f26d-efbb-4abd-802c-3f6a7375ba6a
                Copyright © © 2018 The Authors. Journal of Pharmacy and Pharmacology published by John Wiley & Sons Ltd on behalf of Royal Pharmaceutical Society.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 08 September 2017
                Date accepted : 03 March 2018
                Page count
                Figures: 5, Tables: 1, Pages: 8, Words: 4877
                Categories
                Subject: Research Paper
                Subject: Molecular and Clinical Pharmacology
                Custom metadata
                source-schema-version-number 2.0
                component-id jphp12914
                cover-date July 2018
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.4.3 mode:remove_FC converted:05.07.2018

                Keywords: arthritis,gait,nsaid patch,s (+)‐flurbiprofen plaster
                Data availability:
                Keywords: arthritis, gait, nsaid patch, s (+)‐flurbiprofen plaster

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