Are the anti-inflammatory effects of dexamethasone responsible for inhibition of the induction of enzymes involved in prostanoid formation in rat carrageenin-induced pleurisy?
Since anti-inflammatory steroids modulate multiple gene expression, including the expression of prostaglandin H synthase-2 and phospholipase A 2, at the molecular level, we studied the effects of dexamethasone on rat carrageenin-induced pleurisy to elucidate whether regulation of phospholipase A 2 a...
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| Veröffentlicht in: | European journal of pharmacology 2000-07, Vol.400 (1), p.127-135 |
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| creator | Kawamura, Michiko Hatanaka, Ko Saito, Maki Ogino, Michiko Ono, Takashi Ogino, Keiko Matsuo, Sumitaka Harada, Yoshiteru |
| description | Since anti-inflammatory steroids modulate multiple gene expression, including the expression of prostaglandin H synthase-2 and phospholipase A
2, at the molecular level, we studied the effects of dexamethasone on rat carrageenin-induced pleurisy to elucidate whether regulation of phospholipase A
2 and prostaglandin H synthase-2 expression is the primary mechanism of its anti-inflammatory action. Suppression of plasma exudation by a lower dose of dexamethasone (0.3 mg/kg) was almost equal to that by aspirin (100 mg/kg), but that by higher dexamethasone doses (3 and 30 mg/kg) was considerably stronger, suggesting the involvement of effects other than that on prostanoid formation. The lower dose of dexamethasone also significantly reduced the pleural exudate neutrophil count and prostanoid levels. However, this dose affected neither the prostaglandin H synthase-2 level nor the phospholipase A
2 activity in the exudate cells. The prostaglandin H synthase-2 level was affected only at the higher doses, while phospholipase A
2 activity was not. These results suggest that the anti-inflammatory effects of dexamethasone in acute inflammation cannot be ascribed to direct interference with prostanoid formation via suppression of phospholipase A
2 and prostaglandin H synthase-2 expression. |
| doi_str_mv | 10.1016/S0014-2999(00)00377-0 |
| format | Article |
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2, at the molecular level, we studied the effects of dexamethasone on rat carrageenin-induced pleurisy to elucidate whether regulation of phospholipase A
2 and prostaglandin H synthase-2 expression is the primary mechanism of its anti-inflammatory action. Suppression of plasma exudation by a lower dose of dexamethasone (0.3 mg/kg) was almost equal to that by aspirin (100 mg/kg), but that by higher dexamethasone doses (3 and 30 mg/kg) was considerably stronger, suggesting the involvement of effects other than that on prostanoid formation. The lower dose of dexamethasone also significantly reduced the pleural exudate neutrophil count and prostanoid levels. However, this dose affected neither the prostaglandin H synthase-2 level nor the phospholipase A
2 activity in the exudate cells. The prostaglandin H synthase-2 level was affected only at the higher doses, while phospholipase A
2 activity was not. These results suggest that the anti-inflammatory effects of dexamethasone in acute inflammation cannot be ascribed to direct interference with prostanoid formation via suppression of phospholipase A
2 and prostaglandin H synthase-2 expression.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/S0014-2999(00)00377-0</identifier><identifier>PMID: 10913594</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Anti-inflammatory steroid ; Biological and medical sciences ; Bones, joints and connective tissue. Antiinflammatory agents ; Capillary Permeability - drug effects ; Carrageenin-induced pleurisy ; Dexamethasone ; Dexamethasone - pharmacology ; Dose-Response Relationship, Drug ; Enzyme Induction - drug effects ; Isoenzymes - metabolism ; Male ; Medical sciences ; Neutrophils - drug effects ; Neutrophils - physiology ; Pharmacology. Drug treatments ; Phospholipase A 2 ; Phospholipases A - metabolism ; Pleurisy - drug therapy ; Pleurisy - metabolism ; Prostaglandin H synthase-2 (cyclooxygenase-2) ; Prostaglandin-Endoperoxide Synthases - metabolism ; Prostaglandins - biosynthesis ; rat ; Rats ; Rats, Sprague-Dawley</subject><ispartof>European journal of pharmacology, 2000-07, Vol.400 (1), p.127-135</ispartof><rights>2000 Elsevier Science B.V.</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-afe0410fd8d3cfb086468ab958c92ec2537db4acef509fc3179a47a5fa1c9c413</citedby><cites>FETCH-LOGICAL-c456t-afe0410fd8d3cfb086468ab958c92ec2537db4acef509fc3179a47a5fa1c9c413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0014-2999(00)00377-0$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1428196$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10913594$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kawamura, Michiko</creatorcontrib><creatorcontrib>Hatanaka, Ko</creatorcontrib><creatorcontrib>Saito, Maki</creatorcontrib><creatorcontrib>Ogino, Michiko</creatorcontrib><creatorcontrib>Ono, Takashi</creatorcontrib><creatorcontrib>Ogino, Keiko</creatorcontrib><creatorcontrib>Matsuo, Sumitaka</creatorcontrib><creatorcontrib>Harada, Yoshiteru</creatorcontrib><title>Are the anti-inflammatory effects of dexamethasone responsible for inhibition of the induction of enzymes involved in prostanoid formation in rat carrageenin-induced pleurisy?</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Since anti-inflammatory steroids modulate multiple gene expression, including the expression of prostaglandin H synthase-2 and phospholipase A
2, at the molecular level, we studied the effects of dexamethasone on rat carrageenin-induced pleurisy to elucidate whether regulation of phospholipase A
2 and prostaglandin H synthase-2 expression is the primary mechanism of its anti-inflammatory action. Suppression of plasma exudation by a lower dose of dexamethasone (0.3 mg/kg) was almost equal to that by aspirin (100 mg/kg), but that by higher dexamethasone doses (3 and 30 mg/kg) was considerably stronger, suggesting the involvement of effects other than that on prostanoid formation. The lower dose of dexamethasone also significantly reduced the pleural exudate neutrophil count and prostanoid levels. However, this dose affected neither the prostaglandin H synthase-2 level nor the phospholipase A
2 activity in the exudate cells. The prostaglandin H synthase-2 level was affected only at the higher doses, while phospholipase A
2 activity was not. These results suggest that the anti-inflammatory effects of dexamethasone in acute inflammation cannot be ascribed to direct interference with prostanoid formation via suppression of phospholipase A
2 and prostaglandin H synthase-2 expression.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Anti-inflammatory steroid</subject><subject>Biological and medical sciences</subject><subject>Bones, joints and connective tissue. Antiinflammatory agents</subject><subject>Capillary Permeability - drug effects</subject><subject>Carrageenin-induced pleurisy</subject><subject>Dexamethasone</subject><subject>Dexamethasone - pharmacology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Induction - drug effects</subject><subject>Isoenzymes - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - physiology</subject><subject>Pharmacology. Drug treatments</subject><subject>Phospholipase A 2</subject><subject>Phospholipases A - metabolism</subject><subject>Pleurisy - drug therapy</subject><subject>Pleurisy - metabolism</subject><subject>Prostaglandin H synthase-2 (cyclooxygenase-2)</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Prostaglandins - biosynthesis</subject><subject>rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcuOFDEMRSMEYpqBTwBlgRAsCpx6ZzUajXhJI7EA1pEr5dBBVUmTpFo0P8UvkupuHjtWiazja_texh4LeClAtK8-Aoi6KKWUzwFeAFRdV8AdthF9JwvoRHmXbf4gF-xBjF8BoJFlc59dCJCiamS9YT-vA_G0JY4u2cI6M-E8Y_LhwMkY0ilyb_hI33GmtMXoHfFAceddtMNE3PjArdvawSbr3cquYtaNi_5dIPfjMFPMxb2f9jTmD98FHxM6b8dVIQ9c2VwPmLjGEPALkbOuOArllt1ES7DxcPWQ3TM4RXp0fi_Z5zevP928K24_vH1_c31b6LppU4GGoBZgxn6stBmgb-u2x0E2vZYl6bKpunGoUZNpQBpdiU5i3WFjUGipa1Fdsmcn3bzpt4ViUrONmqYJHfklqmxwK_q-zWBzAnU-KQYyahfsjOGgBKg1KXVMSq0xKAB1TEpB7ntyHrAMM43_dJ2iycDTM4BR42QCOm3jX64ueyHX-VcnjLIbe0tBRW3JZdNsyPGp0dv_bPILGKu1kQ</recordid><startdate>20000714</startdate><enddate>20000714</enddate><creator>Kawamura, Michiko</creator><creator>Hatanaka, Ko</creator><creator>Saito, Maki</creator><creator>Ogino, Michiko</creator><creator>Ono, Takashi</creator><creator>Ogino, Keiko</creator><creator>Matsuo, Sumitaka</creator><creator>Harada, Yoshiteru</creator><general>Elsevier B.V</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>7X8</scope></search><sort><creationdate>20000714</creationdate><title>Are the anti-inflammatory effects of dexamethasone responsible for inhibition of the induction of enzymes involved in prostanoid formation in rat carrageenin-induced pleurisy?</title><author>Kawamura, Michiko ; Hatanaka, Ko ; Saito, Maki ; Ogino, Michiko ; Ono, Takashi ; Ogino, Keiko ; Matsuo, Sumitaka ; Harada, Yoshiteru</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-afe0410fd8d3cfb086468ab958c92ec2537db4acef509fc3179a47a5fa1c9c413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Anti-inflammatory steroid</topic><topic>Biological and medical sciences</topic><topic>Bones, joints and connective tissue. Antiinflammatory agents</topic><topic>Capillary Permeability - drug effects</topic><topic>Carrageenin-induced pleurisy</topic><topic>Dexamethasone</topic><topic>Dexamethasone - pharmacology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Induction - drug effects</topic><topic>Isoenzymes - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - physiology</topic><topic>Pharmacology. Drug treatments</topic><topic>Phospholipase A 2</topic><topic>Phospholipases A - metabolism</topic><topic>Pleurisy - drug therapy</topic><topic>Pleurisy - metabolism</topic><topic>Prostaglandin H synthase-2 (cyclooxygenase-2)</topic><topic>Prostaglandin-Endoperoxide Synthases - metabolism</topic><topic>Prostaglandins - biosynthesis</topic><topic>rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kawamura, Michiko</creatorcontrib><creatorcontrib>Hatanaka, Ko</creatorcontrib><creatorcontrib>Saito, Maki</creatorcontrib><creatorcontrib>Ogino, Michiko</creatorcontrib><creatorcontrib>Ono, Takashi</creatorcontrib><creatorcontrib>Ogino, Keiko</creatorcontrib><creatorcontrib>Matsuo, Sumitaka</creatorcontrib><creatorcontrib>Harada, Yoshiteru</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>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kawamura, Michiko</au><au>Hatanaka, Ko</au><au>Saito, Maki</au><au>Ogino, Michiko</au><au>Ono, Takashi</au><au>Ogino, Keiko</au><au>Matsuo, Sumitaka</au><au>Harada, Yoshiteru</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Are the anti-inflammatory effects of dexamethasone responsible for inhibition of the induction of enzymes involved in prostanoid formation in rat carrageenin-induced pleurisy?</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2000-07-14</date><risdate>2000</risdate><volume>400</volume><issue>1</issue><spage>127</spage><epage>135</epage><pages>127-135</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Since anti-inflammatory steroids modulate multiple gene expression, including the expression of prostaglandin H synthase-2 and phospholipase A
2, at the molecular level, we studied the effects of dexamethasone on rat carrageenin-induced pleurisy to elucidate whether regulation of phospholipase A
2 and prostaglandin H synthase-2 expression is the primary mechanism of its anti-inflammatory action. Suppression of plasma exudation by a lower dose of dexamethasone (0.3 mg/kg) was almost equal to that by aspirin (100 mg/kg), but that by higher dexamethasone doses (3 and 30 mg/kg) was considerably stronger, suggesting the involvement of effects other than that on prostanoid formation. The lower dose of dexamethasone also significantly reduced the pleural exudate neutrophil count and prostanoid levels. However, this dose affected neither the prostaglandin H synthase-2 level nor the phospholipase A
2 activity in the exudate cells. The prostaglandin H synthase-2 level was affected only at the higher doses, while phospholipase A
2 activity was not. These results suggest that the anti-inflammatory effects of dexamethasone in acute inflammation cannot be ascribed to direct interference with prostanoid formation via suppression of phospholipase A
2 and prostaglandin H synthase-2 expression.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>10913594</pmid><doi>10.1016/S0014-2999(00)00377-0</doi><tpages>9</tpages></addata></record> |
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| ispartof | European journal of pharmacology, 2000-07, Vol.400 (1), p.127-135 |
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| subjects | Animals Anti-Inflammatory Agents - pharmacology Anti-inflammatory steroid Biological and medical sciences Bones, joints and connective tissue. Antiinflammatory agents Capillary Permeability - drug effects Carrageenin-induced pleurisy Dexamethasone Dexamethasone - pharmacology Dose-Response Relationship, Drug Enzyme Induction - drug effects Isoenzymes - metabolism Male Medical sciences Neutrophils - drug effects Neutrophils - physiology Pharmacology. Drug treatments Phospholipase A 2 Phospholipases A - metabolism Pleurisy - drug therapy Pleurisy - metabolism Prostaglandin H synthase-2 (cyclooxygenase-2) Prostaglandin-Endoperoxide Synthases - metabolism Prostaglandins - biosynthesis rat Rats Rats, Sprague-Dawley |
| title | Are the anti-inflammatory effects of dexamethasone responsible for inhibition of the induction of enzymes involved in prostanoid formation in rat carrageenin-induced pleurisy? |
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