Anti-allodynic action of the disease-modifying anti-rheumatic drug iguratimod in a rat model of neuropathic pain
Objective Patients with rheumatoid arthritis experience nociceptive as well as neuropathic pain. The effect of iguratimod (IGU), a disease-modifying anti-rheumatic drug, on neuropathic pain in a rat model of chronic constriction injury (CCI) was examined in this study. Methods CCI was induced by mak...
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| Veröffentlicht in: | Inflammation research 2017-10, Vol.66 (10), p.855-862 |
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| creator | Morimoto, K. Miura, A. Tanaka, Keiichi |
| description | Objective
Patients with rheumatoid arthritis experience nociceptive as well as neuropathic pain. The effect of iguratimod (IGU), a disease-modifying anti-rheumatic drug, on neuropathic pain in a rat model of chronic constriction injury (CCI) was examined in this study.
Methods
CCI was induced by making four ligations on the left sciatic nerve. Rats with stable signs of static allodynia were selected 2 weeks after the surgery and drug treatments were started (day 0). The test drugs were orally administered once daily for 15 days. The threshold of mechanical pain response in the hind paw was evaluated by the von Frey hair test in a blinded manner. To observe histological changes in the spinal cord, the L4 region was subjected to immunohistochemical analysis for the detection of microglial cells.
Results
IGU showed an anti-allodynic effect on CCI-induced neuropathic pain at days 6 and 14, but not at 90 min after the first administration of IGU. This effect of IGU was observed until day 21. Furthermore, IGU decreased the number of Iba-1-positive cells, which had been increased at the ipsilateral side of the dorsal horn by CCI.
Conclusions
These results suggest that IGU suppresses neuropathic pain via a different mechanism from that of current therapeutics. |
| doi_str_mv | 10.1007/s00011-017-1064-0 |
| format | Article |
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Patients with rheumatoid arthritis experience nociceptive as well as neuropathic pain. The effect of iguratimod (IGU), a disease-modifying anti-rheumatic drug, on neuropathic pain in a rat model of chronic constriction injury (CCI) was examined in this study.
Methods
CCI was induced by making four ligations on the left sciatic nerve. Rats with stable signs of static allodynia were selected 2 weeks after the surgery and drug treatments were started (day 0). The test drugs were orally administered once daily for 15 days. The threshold of mechanical pain response in the hind paw was evaluated by the von Frey hair test in a blinded manner. To observe histological changes in the spinal cord, the L4 region was subjected to immunohistochemical analysis for the detection of microglial cells.
Results
IGU showed an anti-allodynic effect on CCI-induced neuropathic pain at days 6 and 14, but not at 90 min after the first administration of IGU. This effect of IGU was observed until day 21. Furthermore, IGU decreased the number of Iba-1-positive cells, which had been increased at the ipsilateral side of the dorsal horn by CCI.
Conclusions
These results suggest that IGU suppresses neuropathic pain via a different mechanism from that of current therapeutics.</description><identifier>ISSN: 1023-3830</identifier><identifier>EISSN: 1420-908X</identifier><identifier>DOI: 10.1007/s00011-017-1064-0</identifier><identifier>PMID: 28612120</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Allergology ; Arthritis ; Biomedical and Life Sciences ; Biomedicine ; Dermatology ; Dorsal horn ; Drugs ; Hair ; Immunology ; Microglial cells ; Neuralgia ; Neurology ; Oral administration ; Original Research Paper ; Pain ; Pain perception ; Pharmacology/Toxicology ; Rats ; Rheumatoid arthritis ; Rheumatology ; Rodents ; Sciatic nerve ; Spinal cord ; Surgery</subject><ispartof>Inflammation research, 2017-10, Vol.66 (10), p.855-862</ispartof><rights>Springer International Publishing AG 2017</rights><rights>Inflammation Research is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-70d33c105ab793997a1dd8b838877cb149831f9785d5feca8e36a709222915e3</citedby><cites>FETCH-LOGICAL-c438t-70d33c105ab793997a1dd8b838877cb149831f9785d5feca8e36a709222915e3</cites><orcidid>0000-0002-7950-2438</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00011-017-1064-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00011-017-1064-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28612120$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morimoto, K.</creatorcontrib><creatorcontrib>Miura, A.</creatorcontrib><creatorcontrib>Tanaka, Keiichi</creatorcontrib><title>Anti-allodynic action of the disease-modifying anti-rheumatic drug iguratimod in a rat model of neuropathic pain</title><title>Inflammation research</title><addtitle>Inflamm. Res</addtitle><addtitle>Inflamm Res</addtitle><description>Objective
Patients with rheumatoid arthritis experience nociceptive as well as neuropathic pain. The effect of iguratimod (IGU), a disease-modifying anti-rheumatic drug, on neuropathic pain in a rat model of chronic constriction injury (CCI) was examined in this study.
Methods
CCI was induced by making four ligations on the left sciatic nerve. Rats with stable signs of static allodynia were selected 2 weeks after the surgery and drug treatments were started (day 0). The test drugs were orally administered once daily for 15 days. The threshold of mechanical pain response in the hind paw was evaluated by the von Frey hair test in a blinded manner. To observe histological changes in the spinal cord, the L4 region was subjected to immunohistochemical analysis for the detection of microglial cells.
Results
IGU showed an anti-allodynic effect on CCI-induced neuropathic pain at days 6 and 14, but not at 90 min after the first administration of IGU. This effect of IGU was observed until day 21. Furthermore, IGU decreased the number of Iba-1-positive cells, which had been increased at the ipsilateral side of the dorsal horn by CCI.
Conclusions
These results suggest that IGU suppresses neuropathic pain via a different mechanism from that of current therapeutics.</description><subject>Allergology</subject><subject>Arthritis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Dermatology</subject><subject>Dorsal horn</subject><subject>Drugs</subject><subject>Hair</subject><subject>Immunology</subject><subject>Microglial cells</subject><subject>Neuralgia</subject><subject>Neurology</subject><subject>Oral administration</subject><subject>Original Research Paper</subject><subject>Pain</subject><subject>Pain perception</subject><subject>Pharmacology/Toxicology</subject><subject>Rats</subject><subject>Rheumatoid arthritis</subject><subject>Rheumatology</subject><subject>Rodents</subject><subject>Sciatic nerve</subject><subject>Spinal cord</subject><subject>Surgery</subject><issn>1023-3830</issn><issn>1420-908X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kU9r3DAQxUVJaf60H6CXIOilFyUzkr2SjiGkTSCQSw69Ca0l7yrYkivZh_32ldk0lEJOMw_95o2YR8hXhCsEkNcFABAZoGQIm4bBB3KGDQemQf06qT1wwYQScErOS3mptOKKfyKnXG2QI4czMt3EOTA7DMkdYuio7eaQIk09nfeeulC8LZ6NyYX-EOKO2hXPe7-Mdq64y8uOht2Sq6oQDZFaWgWtwg-rTfRLTpOd95WebIifycfeDsV_ea0X5PnH3fPtPXt8-vlwe_PIukaomUlwQnQIrd1KLbSWFp1TWyWUkrLbYqOVwF5L1bq2951VXmysBM0519h6cUG-H22nnH4vvsxmDKXzw2CjT0sxqEHLRmiOFf32H_qSlhzr5ypVr6ebTbtSeKS6nErJvjdTDqPNB4Ng1jTMMQ1T0zBrGgbqzOWr87IdvXub-Hv-CvAjUOpT3Pn8z-p3Xf8AicyUSA</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Morimoto, K.</creator><creator>Miura, A.</creator><creator>Tanaka, Keiichi</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7950-2438</orcidid></search><sort><creationdate>20171001</creationdate><title>Anti-allodynic action of the disease-modifying anti-rheumatic drug iguratimod in a rat model of neuropathic pain</title><author>Morimoto, K. ; Miura, A. ; Tanaka, Keiichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-70d33c105ab793997a1dd8b838877cb149831f9785d5feca8e36a709222915e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Allergology</topic><topic>Arthritis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Dermatology</topic><topic>Dorsal horn</topic><topic>Drugs</topic><topic>Hair</topic><topic>Immunology</topic><topic>Microglial cells</topic><topic>Neuralgia</topic><topic>Neurology</topic><topic>Oral administration</topic><topic>Original Research Paper</topic><topic>Pain</topic><topic>Pain perception</topic><topic>Pharmacology/Toxicology</topic><topic>Rats</topic><topic>Rheumatoid arthritis</topic><topic>Rheumatology</topic><topic>Rodents</topic><topic>Sciatic nerve</topic><topic>Spinal cord</topic><topic>Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morimoto, K.</creatorcontrib><creatorcontrib>Miura, A.</creatorcontrib><creatorcontrib>Tanaka, Keiichi</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Inflammation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morimoto, K.</au><au>Miura, A.</au><au>Tanaka, Keiichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-allodynic action of the disease-modifying anti-rheumatic drug iguratimod in a rat model of neuropathic pain</atitle><jtitle>Inflammation research</jtitle><stitle>Inflamm. Res</stitle><addtitle>Inflamm Res</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>66</volume><issue>10</issue><spage>855</spage><epage>862</epage><pages>855-862</pages><issn>1023-3830</issn><eissn>1420-908X</eissn><abstract>Objective
Patients with rheumatoid arthritis experience nociceptive as well as neuropathic pain. The effect of iguratimod (IGU), a disease-modifying anti-rheumatic drug, on neuropathic pain in a rat model of chronic constriction injury (CCI) was examined in this study.
Methods
CCI was induced by making four ligations on the left sciatic nerve. Rats with stable signs of static allodynia were selected 2 weeks after the surgery and drug treatments were started (day 0). The test drugs were orally administered once daily for 15 days. The threshold of mechanical pain response in the hind paw was evaluated by the von Frey hair test in a blinded manner. To observe histological changes in the spinal cord, the L4 region was subjected to immunohistochemical analysis for the detection of microglial cells.
Results
IGU showed an anti-allodynic effect on CCI-induced neuropathic pain at days 6 and 14, but not at 90 min after the first administration of IGU. This effect of IGU was observed until day 21. Furthermore, IGU decreased the number of Iba-1-positive cells, which had been increased at the ipsilateral side of the dorsal horn by CCI.
Conclusions
These results suggest that IGU suppresses neuropathic pain via a different mechanism from that of current therapeutics.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>28612120</pmid><doi>10.1007/s00011-017-1064-0</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-7950-2438</orcidid></addata></record> |
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| source | Springer Nature - Complete Springer Journals |
| subjects | Allergology Arthritis Biomedical and Life Sciences Biomedicine Dermatology Dorsal horn Drugs Hair Immunology Microglial cells Neuralgia Neurology Oral administration Original Research Paper Pain Pain perception Pharmacology/Toxicology Rats Rheumatoid arthritis Rheumatology Rodents Sciatic nerve Spinal cord Surgery |
| title | Anti-allodynic action of the disease-modifying anti-rheumatic drug iguratimod in a rat model of neuropathic pain |
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