{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T00:59:24Z","timestamp":1778547564470,"version":"3.51.4"},"reference-count":47,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2012,2,21]],"date-time":"2012-02-21T00:00:00Z","timestamp":1329782400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["European Journal of Pain"],"published-print":{"date-parts":[[2012,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Inflammation of the temporomandibular joint (<jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>) induced by rheumatoid arthritis (<jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>) have resulted in persistent pain and caused distress to many patients. Considering that not all patients respond to traditional drugs therapy to <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content> and it has demonstrated that 15\u2010deoxy\u2010<jats:sup>\u039412,14<\/jats:sup>\u2010prostaglandin <jats:styled-content style=\"fixed-case\">J<\/jats:styled-content><jats:sub>2<\/jats:sub> (15<jats:styled-content style=\"fixed-case\">d<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PGJ<\/jats:styled-content><jats:sub>2<\/jats:sub>) into <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> has a potential peripheral antinociceptive effect, the aim of this study was to evaluate the peripheral effect of 15<jats:styled-content style=\"fixed-case\">d<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PGJ<\/jats:styled-content><jats:sub>2<\/jats:sub> in <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> inflammatory hypernociception.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Antigen\u2010induced arthritis (<jats:styled-content style=\"fixed-case\">AIA<\/jats:styled-content>) was generated in rats with methylated bovine serum albumin (<jats:styled-content style=\"fixed-case\">mBSA<\/jats:styled-content>). <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> hypernociception was assessed by measuring the behavioural nociceptive responses. After behavioural experiments, the animals were terminally anaesthetized and periarticular tissues were removed and homogenized. The supernatants were used to evaluate the levels of tumour necrosis factor (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>)\u2010\u03b1, interleukin (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>)\u20101\u03b2 and keratinocyte\u2010derived chemokine (<jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content>) by enzyme\u2010linked immunosorbent assay as well the expression of <jats:styled-content style=\"fixed-case\">PKC<\/jats:styled-content>\u03b5 and <jats:styled-content style=\"fixed-case\">PKA<\/jats:styled-content> by western blotting analysis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The intra\u2010articular injection of <jats:styled-content style=\"fixed-case\">mBSA<\/jats:styled-content>, but not phosphate buffered saline (control), in immunized rats induced dose\u2010 and time\u2010dependent behavioural nociceptive responses in which the peak of nociceptive responses were obtained by using 10\u2009\u03bcg\/<jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> of <jats:styled-content style=\"fixed-case\">mBSA<\/jats:styled-content> after 24\u2009h. Pretreatment with 15<jats:styled-content style=\"fixed-case\">d<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PGJ<\/jats:styled-content><jats:sub>2<\/jats:sub> (30, 100 and 300\u2009ng\/<jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>) inhibited the <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> inflammatory hypernociception. In addition, 15<jats:styled-content style=\"fixed-case\">d<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PGJ<\/jats:styled-content><jats:sub>2<\/jats:sub> reduced the <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\u2010induced release of <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 and <jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content> (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) as well the expression of <jats:styled-content style=\"fixed-case\">PKA<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">PKC<\/jats:styled-content>\u03b5 (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>In the present study, we demonstrated that 15<jats:styled-content style=\"fixed-case\">d<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PGJ<\/jats:styled-content><jats:sub>2<\/jats:sub> was able to reduce the <jats:styled-content style=\"fixed-case\">RA<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content> inflammatory hypernociception by an indirect mechanism. This antinociceptive effect is in part due to decrease of <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>\u2010\u03b1, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2 and <jats:styled-content style=\"fixed-case\">KC<\/jats:styled-content> levels and <jats:styled-content style=\"fixed-case\">PKA<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PKC<\/jats:styled-content>\u03b5 expression in the <jats:styled-content style=\"fixed-case\">TMJ<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1002\/j.1532-2149.2012.00114.x","type":"journal-article","created":{"date-parts":[[2012,2,21]],"date-time":"2012-02-21T17:25:17Z","timestamp":1329845117000},"page":"1106-1115","source":"Crossref","is-referenced-by-count":23,"title":["The indirect antinociceptive mechanism of 15<scp>d<\/scp>\u2010<scp>PGJ<\/scp><sub>2<\/sub> on rheumatoid arthritis\u2010induced <scp>TMJ<\/scp> inflammatory pain in 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