Dexamethasone prevents the induction of COX-2 mRNA and prostaglandins in the lumbar spinal cord following intraplantar FCA in parallel with inhibition of oedema
The inducible form of cyclo-oxygenase (COX-2) mRNA is rapidly induced in the spinal cord following peripheral inflammation produced by intraplantar injection of Freund’s complete adjuvant (FCA). COX-2 mRNA induction is also accompanied by increased prostaglandin (PG) levels which are closely correla...
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| Veröffentlicht in: | Neuropharmacology 1998-06, Vol.37 (6), p.739-744 |
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| creator | Hay, C.H de Belleroche, J.S |
| description | The inducible form of cyclo-oxygenase (COX-2) mRNA is rapidly induced in the spinal cord following peripheral inflammation produced by intraplantar injection of Freund’s complete adjuvant (FCA). COX-2 mRNA induction is also accompanied by increased prostaglandin (PG) levels which are closely correlated with behavioural indicators of increased pain sensitivity. The aim of this study was to determine whether the anti-inflammatory glucocorticoid, dexamethasone, which acts locally to prevent the development of oedema would also reduce the associated central changes characterised by the induction of COX-2 mRNA and PGs. Unilateral intraplantar FCA induced a marked oedema evident from 2 h to 7 days after FCA injection which was significantly attenuated by dexamethasone pretreatment at all time points. Dexamethasone also significantly prevented the induction of COX-2 mRNA (2–4 h) and elevated levels of prostaglandins (6-keto PGF
1α) in lumbar spinal cord (8 h). In this study we have confirmed the anti-inflammatory effect of dexamethasone and linked this to central changes in gene expression relevant to the development of altered pain thresholds following intraplantar FCA. |
| doi_str_mv | 10.1016/S0028-3908(98)00073-2 |
| format | Article |
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1α) in lumbar spinal cord (8 h). In this study we have confirmed the anti-inflammatory effect of dexamethasone and linked this to central changes in gene expression relevant to the development of altered pain thresholds following intraplantar FCA.</description><identifier>ISSN: 0028-3908</identifier><identifier>EISSN: 1873-7064</identifier><identifier>DOI: 10.1016/S0028-3908(98)00073-2</identifier><identifier>PMID: 9707287</identifier><identifier>CODEN: NEPHBW</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-Inflammatory Agents - therapeutic use ; Biological and medical sciences ; Bones, joints and connective tissue. Antiinflammatory agents ; Cyclo-oxygenase-2 ; Cyclooxygenase 2 ; Dexamethasone ; Dexamethasone - pharmacology ; Dexamethasone - therapeutic use ; Edema - chemically induced ; Edema - prevention & control ; Freund's Adjuvant ; Glucocorticoids - pharmacology ; Glucocorticoids - therapeutic use ; Inflammation ; Injections, Spinal ; Isoenzymes - biosynthesis ; Male ; Medical sciences ; mRNA ; Oedema ; Pharmacology. Drug treatments ; Prostaglandin-Endoperoxide Synthases - biosynthesis ; Prostaglandins ; Prostaglandins - biosynthesis ; Rats ; RNA, Messenger - metabolism ; Spinal cord ; Spinal Cord - drug effects ; Spinal Cord - metabolism ; Spinal Cord Diseases - chemically induced ; Spinal Cord Diseases - prevention & control</subject><ispartof>Neuropharmacology, 1998-06, Vol.37 (6), p.739-744</ispartof><rights>1998 Elsevier Science Ltd</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-5b1e9ce1077afd1f591449faf5ecbade800e9f025395f9f2685878c005e6d5893</citedby><cites>FETCH-LOGICAL-c420t-5b1e9ce1077afd1f591449faf5ecbade800e9f025395f9f2685878c005e6d5893</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0028390898000732$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,65309</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2379475$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9707287$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hay, C.H</creatorcontrib><creatorcontrib>de Belleroche, J.S</creatorcontrib><title>Dexamethasone prevents the induction of COX-2 mRNA and prostaglandins in the lumbar spinal cord following intraplantar FCA in parallel with inhibition of oedema</title><title>Neuropharmacology</title><addtitle>Neuropharmacology</addtitle><description>The inducible form of cyclo-oxygenase (COX-2) mRNA is rapidly induced in the spinal cord following peripheral inflammation produced by intraplantar injection of Freund’s complete adjuvant (FCA). COX-2 mRNA induction is also accompanied by increased prostaglandin (PG) levels which are closely correlated with behavioural indicators of increased pain sensitivity. The aim of this study was to determine whether the anti-inflammatory glucocorticoid, dexamethasone, which acts locally to prevent the development of oedema would also reduce the associated central changes characterised by the induction of COX-2 mRNA and PGs. Unilateral intraplantar FCA induced a marked oedema evident from 2 h to 7 days after FCA injection which was significantly attenuated by dexamethasone pretreatment at all time points. Dexamethasone also significantly prevented the induction of COX-2 mRNA (2–4 h) and elevated levels of prostaglandins (6-keto PGF
1α) in lumbar spinal cord (8 h). In this study we have confirmed the anti-inflammatory effect of dexamethasone and linked this to central changes in gene expression relevant to the development of altered pain thresholds following intraplantar FCA.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Bones, joints and connective tissue. Antiinflammatory agents</subject><subject>Cyclo-oxygenase-2</subject><subject>Cyclooxygenase 2</subject><subject>Dexamethasone</subject><subject>Dexamethasone - pharmacology</subject><subject>Dexamethasone - therapeutic use</subject><subject>Edema - chemically induced</subject><subject>Edema - prevention & control</subject><subject>Freund's Adjuvant</subject><subject>Glucocorticoids - pharmacology</subject><subject>Glucocorticoids - therapeutic use</subject><subject>Inflammation</subject><subject>Injections, Spinal</subject><subject>Isoenzymes - biosynthesis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>mRNA</subject><subject>Oedema</subject><subject>Pharmacology. Drug treatments</subject><subject>Prostaglandin-Endoperoxide Synthases - biosynthesis</subject><subject>Prostaglandins</subject><subject>Prostaglandins - biosynthesis</subject><subject>Rats</subject><subject>RNA, Messenger - metabolism</subject><subject>Spinal cord</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - metabolism</subject><subject>Spinal Cord Diseases - chemically induced</subject><subject>Spinal Cord Diseases - prevention & control</subject><issn>0028-3908</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcuOFCEUhonRjD2tjzAJC2N0UQpVRQMr02kdNZk4iZfEHaHgMI2hLgPUjPM2Pqr0xd664oTz_ZzD_yN0QckbSujq7TdCalE1kohXUrwmhPCmqh-hBRWl4GTVPkaLE_IUnaf0q0CtoOIMnUlOeC34Av15D791D3mr0zgAniLcwZATzlvAfrCzyX4c8Ojw5vpnVeP-65c11oMt4Jiyvgml9kMq6F4R5r7TEafJDzpgM0aL3RjCeO-Hm8LkqKeiyAW53Kx3oklHHQIEfO_ztlxsfef_TRzBQq-foSdOhwTPj-cS_bj88H3zqbq6_vh5s76qTFuTXLGOgjRACefaWeqYpG0rnXYMTKctCEJAOlKzRjInXb0STHBhCGGwskzIZoleHt4tP7udIWXV-2QglH1hnJOinLZ8Z_ISsQNoigUpglNT9L2OD4oStUtG7ZNRO9uVFGqfjKqL7uI4YO56sCfVMYrSf3Hs62R0cFEPxqcTVjdctpwV7N0Bg2LGnYeokvEwGLA-gsnKjv4_i_wFAwOs3A</recordid><startdate>19980601</startdate><enddate>19980601</enddate><creator>Hay, C.H</creator><creator>de Belleroche, J.S</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>19980601</creationdate><title>Dexamethasone prevents the induction of COX-2 mRNA and prostaglandins in the lumbar spinal cord following intraplantar FCA in parallel with inhibition of oedema</title><author>Hay, C.H ; de Belleroche, J.S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-5b1e9ce1077afd1f591449faf5ecbade800e9f025395f9f2685878c005e6d5893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Bones, joints and connective tissue. Antiinflammatory agents</topic><topic>Cyclo-oxygenase-2</topic><topic>Cyclooxygenase 2</topic><topic>Dexamethasone</topic><topic>Dexamethasone - pharmacology</topic><topic>Dexamethasone - therapeutic use</topic><topic>Edema - chemically induced</topic><topic>Edema - prevention & control</topic><topic>Freund's Adjuvant</topic><topic>Glucocorticoids - pharmacology</topic><topic>Glucocorticoids - therapeutic use</topic><topic>Inflammation</topic><topic>Injections, Spinal</topic><topic>Isoenzymes - biosynthesis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>mRNA</topic><topic>Oedema</topic><topic>Pharmacology. Drug treatments</topic><topic>Prostaglandin-Endoperoxide Synthases - biosynthesis</topic><topic>Prostaglandins</topic><topic>Prostaglandins - biosynthesis</topic><topic>Rats</topic><topic>RNA, Messenger - metabolism</topic><topic>Spinal cord</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - metabolism</topic><topic>Spinal Cord Diseases - chemically induced</topic><topic>Spinal Cord Diseases - prevention & control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hay, C.H</creatorcontrib><creatorcontrib>de Belleroche, J.S</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Neuropharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hay, C.H</au><au>de Belleroche, J.S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dexamethasone prevents the induction of COX-2 mRNA and prostaglandins in the lumbar spinal cord following intraplantar FCA in parallel with inhibition of oedema</atitle><jtitle>Neuropharmacology</jtitle><addtitle>Neuropharmacology</addtitle><date>1998-06-01</date><risdate>1998</risdate><volume>37</volume><issue>6</issue><spage>739</spage><epage>744</epage><pages>739-744</pages><issn>0028-3908</issn><eissn>1873-7064</eissn><coden>NEPHBW</coden><abstract>The inducible form of cyclo-oxygenase (COX-2) mRNA is rapidly induced in the spinal cord following peripheral inflammation produced by intraplantar injection of Freund’s complete adjuvant (FCA). COX-2 mRNA induction is also accompanied by increased prostaglandin (PG) levels which are closely correlated with behavioural indicators of increased pain sensitivity. The aim of this study was to determine whether the anti-inflammatory glucocorticoid, dexamethasone, which acts locally to prevent the development of oedema would also reduce the associated central changes characterised by the induction of COX-2 mRNA and PGs. Unilateral intraplantar FCA induced a marked oedema evident from 2 h to 7 days after FCA injection which was significantly attenuated by dexamethasone pretreatment at all time points. Dexamethasone also significantly prevented the induction of COX-2 mRNA (2–4 h) and elevated levels of prostaglandins (6-keto PGF
1α) in lumbar spinal cord (8 h). In this study we have confirmed the anti-inflammatory effect of dexamethasone and linked this to central changes in gene expression relevant to the development of altered pain thresholds following intraplantar FCA.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>9707287</pmid><doi>10.1016/S0028-3908(98)00073-2</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Anti-Inflammatory Agents - pharmacology Anti-Inflammatory Agents - therapeutic use Biological and medical sciences Bones, joints and connective tissue. Antiinflammatory agents Cyclo-oxygenase-2 Cyclooxygenase 2 Dexamethasone Dexamethasone - pharmacology Dexamethasone - therapeutic use Edema - chemically induced Edema - prevention & control Freund's Adjuvant Glucocorticoids - pharmacology Glucocorticoids - therapeutic use Inflammation Injections, Spinal Isoenzymes - biosynthesis Male Medical sciences mRNA Oedema Pharmacology. Drug treatments Prostaglandin-Endoperoxide Synthases - biosynthesis Prostaglandins Prostaglandins - biosynthesis Rats RNA, Messenger - metabolism Spinal cord Spinal Cord - drug effects Spinal Cord - metabolism Spinal Cord Diseases - chemically induced Spinal Cord Diseases - prevention & control |
| title | Dexamethasone prevents the induction of COX-2 mRNA and prostaglandins in the lumbar spinal cord following intraplantar FCA in parallel with inhibition of oedema |
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