Intra-articular administration of tachykinin NK sub(1 receptor antagonists reduces hyperalgesia and cartilage destruction in the inflammatory joint in rats with adjuvant-induced arthritis)
Persistent pain associated with inflammatory arthritis is an aggravating factor that decreases patients' quality of life. Current therapies for joint pain have limited effectiveness and produce unwanted negative side effects. Although the involvement of substance P and its cognate tachykinin re...
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Veröffentlicht in: | European journal of pharmacology 2011-10, Vol.668 (1-2), p.163-168 |
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creator | Uematsu, Takuya Sakai, Atsushi Ito, Hiromoto Suzuki, Hidenori |
description | Persistent pain associated with inflammatory arthritis is an aggravating factor that decreases patients' quality of life. Current therapies for joint pain have limited effectiveness and produce unwanted negative side effects. Although the involvement of substance P and its cognate tachykinin receptor, NK sub(1, in joint inflammation has been extensively documented through animal experiments, the development of oral tachykinin NK) sub(1) receptor antagonists against arthritis-induced pain has been unsuccessful in humans to date. To explore the possibility of using tachykinin NK sub(1 receptor antagonists as local therapeutic agents for inflammatory arthritis, we examined the effects of tachykinin NK) sub(1) receptor antagonists administered into the rat ankle joint on hyperalgesia in complete Freund's adjuvant (CFA)-induced inflammatory monoarthritis. Administration of the tachykinin NK sub(1 receptor antagonist WIN 51708 or GR 82334 into the affected ankle joint at day 3 following intra-articular CFA injection reduced the mechanical hyperalgesia 12 h after the tachykinin NK) sub(1) receptor antagonist injection and their analgesic effects persisted for at least 2 days. Histological examinations revealed that intra-articular WIN 51708 reduced the CFA-induced destructive changes in the cartilage. These findings suggest that intra-articular injection of tachykinin NK sub(1 receptor antagonists is a promising strategy for relieving the hyperalgesia that occurs in inflammatory arthritis.) |
doi_str_mv | 10.1016/j.ejphar.2011.06.037 |
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Current therapies for joint pain have limited effectiveness and produce unwanted negative side effects. Although the involvement of substance P and its cognate tachykinin receptor, NK sub(1, in joint inflammation has been extensively documented through animal experiments, the development of oral tachykinin NK) sub(1) receptor antagonists against arthritis-induced pain has been unsuccessful in humans to date. To explore the possibility of using tachykinin NK sub(1 receptor antagonists as local therapeutic agents for inflammatory arthritis, we examined the effects of tachykinin NK) sub(1) receptor antagonists administered into the rat ankle joint on hyperalgesia in complete Freund's adjuvant (CFA)-induced inflammatory monoarthritis. Administration of the tachykinin NK sub(1 receptor antagonist WIN 51708 or GR 82334 into the affected ankle joint at day 3 following intra-articular CFA injection reduced the mechanical hyperalgesia 12 h after the tachykinin NK) sub(1) receptor antagonist injection and their analgesic effects persisted for at least 2 days. Histological examinations revealed that intra-articular WIN 51708 reduced the CFA-induced destructive changes in the cartilage. These findings suggest that intra-articular injection of tachykinin NK sub(1 receptor antagonists is a promising strategy for relieving the hyperalgesia that occurs in inflammatory arthritis.)</description><identifier>ISSN: 0014-2999</identifier><identifier>DOI: 10.1016/j.ejphar.2011.06.037</identifier><language>eng</language><subject>Analgesics ; Ankle ; Antagonists ; Arthritis ; Cartilage ; Freund's adjuvant ; Inflammation ; Joint diseases ; Neurokinin NK1 receptors ; Pain perception ; Quality of life ; Side effects ; Substance P ; Tachykinin ; tachykinin receptors</subject><ispartof>European journal of pharmacology, 2011-10, Vol.668 (1-2), p.163-168</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids></links><search><creatorcontrib>Uematsu, Takuya</creatorcontrib><creatorcontrib>Sakai, Atsushi</creatorcontrib><creatorcontrib>Ito, Hiromoto</creatorcontrib><creatorcontrib>Suzuki, Hidenori</creatorcontrib><title>Intra-articular administration of tachykinin NK sub(1 receptor antagonists reduces hyperalgesia and cartilage destruction in the inflammatory joint in rats with adjuvant-induced arthritis)</title><title>European journal of pharmacology</title><description>Persistent pain associated with inflammatory arthritis is an aggravating factor that decreases patients' quality of life. Current therapies for joint pain have limited effectiveness and produce unwanted negative side effects. Although the involvement of substance P and its cognate tachykinin receptor, NK sub(1, in joint inflammation has been extensively documented through animal experiments, the development of oral tachykinin NK) sub(1) receptor antagonists against arthritis-induced pain has been unsuccessful in humans to date. To explore the possibility of using tachykinin NK sub(1 receptor antagonists as local therapeutic agents for inflammatory arthritis, we examined the effects of tachykinin NK) sub(1) receptor antagonists administered into the rat ankle joint on hyperalgesia in complete Freund's adjuvant (CFA)-induced inflammatory monoarthritis. Administration of the tachykinin NK sub(1 receptor antagonist WIN 51708 or GR 82334 into the affected ankle joint at day 3 following intra-articular CFA injection reduced the mechanical hyperalgesia 12 h after the tachykinin NK) sub(1) receptor antagonist injection and their analgesic effects persisted for at least 2 days. Histological examinations revealed that intra-articular WIN 51708 reduced the CFA-induced destructive changes in the cartilage. These findings suggest that intra-articular injection of tachykinin NK sub(1 receptor antagonists is a promising strategy for relieving the hyperalgesia that occurs in inflammatory arthritis.)</description><subject>Analgesics</subject><subject>Ankle</subject><subject>Antagonists</subject><subject>Arthritis</subject><subject>Cartilage</subject><subject>Freund's adjuvant</subject><subject>Inflammation</subject><subject>Joint diseases</subject><subject>Neurokinin NK1 receptors</subject><subject>Pain perception</subject><subject>Quality of life</subject><subject>Side effects</subject><subject>Substance P</subject><subject>Tachykinin</subject><subject>tachykinin receptors</subject><issn>0014-2999</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqVjr1OxDAQhF2AxPHzBhQujyLBTnJ3pEYg0ElU9KfFcWIHxw5eG3TvxsOxQbwA1Uizs98MY9dSlFLI7e1Y6nE2EMtKSFmKbSnq3QlbCSGbomrb9oydI45CiE1bbVbs-9mnCAXEZFV2EDl0k_UWyUw2eB56nkCZ4zuZnr_sOea3teRRKz2nQHGfYAjLA5LZZaWRm-OsI7hBowUKdFwteAeD5p0mcla_aOIlo0l6B9MERDvyMViflgvVI_-yydCgMX9STWH9gu84wUy0yeLNJTvtwaG--tMLtn58eL1_KuYYPjJVHSaLSjsHXoeMBynaumnuZLOr_xH9AXR2c2U</recordid><startdate>20111001</startdate><enddate>20111001</enddate><creator>Uematsu, Takuya</creator><creator>Sakai, Atsushi</creator><creator>Ito, Hiromoto</creator><creator>Suzuki, Hidenori</creator><scope>7TK</scope></search><sort><creationdate>20111001</creationdate><title>Intra-articular administration of tachykinin NK sub(1 receptor antagonists reduces hyperalgesia and cartilage destruction in the inflammatory joint in rats with adjuvant-induced arthritis)</title><author>Uematsu, Takuya ; Sakai, Atsushi ; Ito, Hiromoto ; Suzuki, Hidenori</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_miscellaneous_10934481473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Analgesics</topic><topic>Ankle</topic><topic>Antagonists</topic><topic>Arthritis</topic><topic>Cartilage</topic><topic>Freund's adjuvant</topic><topic>Inflammation</topic><topic>Joint diseases</topic><topic>Neurokinin NK1 receptors</topic><topic>Pain perception</topic><topic>Quality of life</topic><topic>Side effects</topic><topic>Substance P</topic><topic>Tachykinin</topic><topic>tachykinin receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Uematsu, Takuya</creatorcontrib><creatorcontrib>Sakai, Atsushi</creatorcontrib><creatorcontrib>Ito, Hiromoto</creatorcontrib><creatorcontrib>Suzuki, Hidenori</creatorcontrib><collection>Neurosciences Abstracts</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Uematsu, Takuya</au><au>Sakai, Atsushi</au><au>Ito, Hiromoto</au><au>Suzuki, Hidenori</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intra-articular administration of tachykinin NK sub(1 receptor antagonists reduces hyperalgesia and cartilage destruction in the inflammatory joint in rats with adjuvant-induced arthritis)</atitle><jtitle>European journal of pharmacology</jtitle><date>2011-10-01</date><risdate>2011</risdate><volume>668</volume><issue>1-2</issue><spage>163</spage><epage>168</epage><pages>163-168</pages><issn>0014-2999</issn><abstract>Persistent pain associated with inflammatory arthritis is an aggravating factor that decreases patients' quality of life. Current therapies for joint pain have limited effectiveness and produce unwanted negative side effects. Although the involvement of substance P and its cognate tachykinin receptor, NK sub(1, in joint inflammation has been extensively documented through animal experiments, the development of oral tachykinin NK) sub(1) receptor antagonists against arthritis-induced pain has been unsuccessful in humans to date. To explore the possibility of using tachykinin NK sub(1 receptor antagonists as local therapeutic agents for inflammatory arthritis, we examined the effects of tachykinin NK) sub(1) receptor antagonists administered into the rat ankle joint on hyperalgesia in complete Freund's adjuvant (CFA)-induced inflammatory monoarthritis. Administration of the tachykinin NK sub(1 receptor antagonist WIN 51708 or GR 82334 into the affected ankle joint at day 3 following intra-articular CFA injection reduced the mechanical hyperalgesia 12 h after the tachykinin NK) sub(1) receptor antagonist injection and their analgesic effects persisted for at least 2 days. Histological examinations revealed that intra-articular WIN 51708 reduced the CFA-induced destructive changes in the cartilage. These findings suggest that intra-articular injection of tachykinin NK sub(1 receptor antagonists is a promising strategy for relieving the hyperalgesia that occurs in inflammatory arthritis.)</abstract><doi>10.1016/j.ejphar.2011.06.037</doi></addata></record> |
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subjects | Analgesics Ankle Antagonists Arthritis Cartilage Freund's adjuvant Inflammation Joint diseases Neurokinin NK1 receptors Pain perception Quality of life Side effects Substance P Tachykinin tachykinin receptors |
title | Intra-articular administration of tachykinin NK sub(1 receptor antagonists reduces hyperalgesia and cartilage destruction in the inflammatory joint in rats with adjuvant-induced arthritis) |
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