Capsazepine, a vanilloid receptor antagonist, inhibits the expression of inducible nitric oxide synthase gene in lipopolysaccharide-stimulated RAW264.7 macrophages through the inactivation of nuclear transcription factor-kappa B
High amounts of nitric oxide (NO) production following the induction of inducible NO synthase (iNOS) gene expression has been implicated in the pathogenesis of inflammatory diseases. Capsaicin, a vanilloid receptor agonist, is known to have an inhibitory effect on NO production in macrophages. In th...
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| Veröffentlicht in: | International immunopharmacology 2001-04, Vol.1 (4), p.777-784 |
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| creator | Oh, Gi-Su Pae, Hyun-Ock Seo, Won-Gil Kim, Na-Young Pyun, Kwang Ho Kim, Il-Kwang Shin, Min-kyo Chung, Hun-Taeg |
| description | High amounts of nitric oxide (NO) production following the induction of inducible NO synthase (iNOS) gene expression has been implicated in the pathogenesis of inflammatory diseases. Capsaicin, a vanilloid receptor agonist, is known to have an inhibitory effect on NO production in macrophages. In the present study, we have found that capsazepine (CAPZ), a vanilloid receptor antagonist, also inhibited NO and iNOS protein syntheses induced by lipopolysaccharide in RAW264.7 macrophages via the suppression of iNOS mRNA. The mechanistic studies showed that CAPZ inhibited the expression of iNOS mRNA through the inactivation of nuclear transcription factor-kappa B (NF-κ B). Thus, capsazepine may be a useful candidate for the development of a drug to treat inflammatory diseases related to iNOS gene overexpression. |
| doi_str_mv | 10.1016/S1567-5769(01)00012-1 |
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Capsaicin, a vanilloid receptor agonist, is known to have an inhibitory effect on NO production in macrophages. In the present study, we have found that capsazepine (CAPZ), a vanilloid receptor antagonist, also inhibited NO and iNOS protein syntheses induced by lipopolysaccharide in RAW264.7 macrophages via the suppression of iNOS mRNA. The mechanistic studies showed that CAPZ inhibited the expression of iNOS mRNA through the inactivation of nuclear transcription factor-kappa B (NF-κ B). Thus, capsazepine may be a useful candidate for the development of a drug to treat inflammatory diseases related to iNOS gene overexpression.</description><identifier>ISSN: 1567-5769</identifier><identifier>EISSN: 1878-1705</identifier><identifier>DOI: 10.1016/S1567-5769(01)00012-1</identifier><identifier>PMID: 11357890</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Biological and medical sciences ; Bones, joints and connective tissue. Antiinflammatory agents ; Capsaicin ; Capsaicin - analogs & derivatives ; Capsaicin - pharmacology ; Capsazepine ; Cell Line ; Gene Expression Regulation, Enzymologic - drug effects ; Inducible nitric oxide synthase ; Lipopolysaccharides - pharmacology ; Macrophages - enzymology ; Medical sciences ; Mice ; NF-kappa B - antagonists & inhibitors ; Nitric oxide ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - genetics ; Nitric Oxide Synthase Type II ; Nuclear transcription factor-kappa B ; Pharmacology. Drug treatments ; Receptors, Drug - antagonists & inhibitors ; RNA, Messenger - analysis ; vanilloid receptors</subject><ispartof>International immunopharmacology, 2001-04, Vol.1 (4), p.777-784</ispartof><rights>2001 Elsevier Science B.V.</rights><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c361t-63057c4d24417c23b9da7982b2a3cc8f5cdf1120ac80857552c2e1b14f5100613</citedby><cites>FETCH-LOGICAL-c361t-63057c4d24417c23b9da7982b2a3cc8f5cdf1120ac80857552c2e1b14f5100613</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1567576901000121$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1012580$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11357890$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oh, Gi-Su</creatorcontrib><creatorcontrib>Pae, Hyun-Ock</creatorcontrib><creatorcontrib>Seo, Won-Gil</creatorcontrib><creatorcontrib>Kim, Na-Young</creatorcontrib><creatorcontrib>Pyun, Kwang Ho</creatorcontrib><creatorcontrib>Kim, Il-Kwang</creatorcontrib><creatorcontrib>Shin, Min-kyo</creatorcontrib><creatorcontrib>Chung, Hun-Taeg</creatorcontrib><title>Capsazepine, a vanilloid receptor antagonist, inhibits the expression of inducible nitric oxide synthase gene in lipopolysaccharide-stimulated RAW264.7 macrophages through the inactivation of nuclear transcription factor-kappa B</title><title>International immunopharmacology</title><addtitle>Int Immunopharmacol</addtitle><description>High amounts of nitric oxide (NO) production following the induction of inducible NO synthase (iNOS) gene expression has been implicated in the pathogenesis of inflammatory diseases. Capsaicin, a vanilloid receptor agonist, is known to have an inhibitory effect on NO production in macrophages. In the present study, we have found that capsazepine (CAPZ), a vanilloid receptor antagonist, also inhibited NO and iNOS protein syntheses induced by lipopolysaccharide in RAW264.7 macrophages via the suppression of iNOS mRNA. The mechanistic studies showed that CAPZ inhibited the expression of iNOS mRNA through the inactivation of nuclear transcription factor-kappa B (NF-κ B). Thus, capsazepine may be a useful candidate for the development of a drug to treat inflammatory diseases related to iNOS gene overexpression.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bones, joints and connective tissue. Antiinflammatory agents</subject><subject>Capsaicin</subject><subject>Capsaicin - analogs & derivatives</subject><subject>Capsaicin - pharmacology</subject><subject>Capsazepine</subject><subject>Cell Line</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>Inducible nitric oxide synthase</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Macrophages - enzymology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - genetics</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Nuclear transcription factor-kappa B</subject><subject>Pharmacology. Drug treatments</subject><subject>Receptors, Drug - antagonists & inhibitors</subject><subject>RNA, Messenger - analysis</subject><subject>vanilloid receptors</subject><issn>1567-5769</issn><issn>1878-1705</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkt2KFDEQhRtR3HX1EZRciChsr6nuTqfnStbBP1gQ_MHLUJ2unon2JDFJDzs-rw9iZnZE7_YqgfqqTnHqFMVj4BfAoX35GUQrSyHbxXMOLzjnUJVwpziFTnYlSC7u5v9f5KR4EOP3zEjewP3iBKAWslvw0-L3En3EX-SNpXOGbIvWTJMzAwukyScXGNqEK2dNTOfM2LXpTYosrYnRtQ8Uo3GWuTGXhlmbfiJmTQpGM3dtBmJxZ9MaI7EVWcoQm4x33k27iFqvMWSmjMls5gkTDezT5beqbS4k26AOzq9xRXux4ObV-iBqLOpktpiOsnbWE2FgKaCNOhh_KIwZcqH8gd4je_2wuDfiFOnR8T0rvr5982X5vrz6-O7D8vKq1HULqWxrLqRuhqppQOqq7hcDykVX9RXWWnej0MMIUHHUHe-EFKLSFUEPzSiA8xbqs-LZzVwf3M-ZYlIbEzVNE1pyc1SSd3UtO3krCB2XUFd1BsUNmM2IMdCofDAbDDsFXO1zoA45UPsjKw7qkAO13-TJUWDuNzT86zoePgNPjwBGjdOY3dMm_jcdKtHtsVc3GGXbtoaCitqQ1TSYnI-kBmdu2eQPb-nUbQ</recordid><startdate>200104</startdate><enddate>200104</enddate><creator>Oh, Gi-Su</creator><creator>Pae, Hyun-Ock</creator><creator>Seo, Won-Gil</creator><creator>Kim, Na-Young</creator><creator>Pyun, Kwang Ho</creator><creator>Kim, Il-Kwang</creator><creator>Shin, Min-kyo</creator><creator>Chung, Hun-Taeg</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200104</creationdate><title>Capsazepine, a vanilloid receptor antagonist, inhibits the expression of inducible nitric oxide synthase gene in lipopolysaccharide-stimulated RAW264.7 macrophages through the inactivation of nuclear transcription factor-kappa B</title><author>Oh, Gi-Su ; Pae, Hyun-Ock ; Seo, Won-Gil ; Kim, Na-Young ; Pyun, Kwang Ho ; Kim, Il-Kwang ; Shin, Min-kyo ; Chung, Hun-Taeg</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c361t-63057c4d24417c23b9da7982b2a3cc8f5cdf1120ac80857552c2e1b14f5100613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bones, joints and connective tissue. Antiinflammatory agents</topic><topic>Capsaicin</topic><topic>Capsaicin - analogs & derivatives</topic><topic>Capsaicin - pharmacology</topic><topic>Capsazepine</topic><topic>Cell Line</topic><topic>Gene Expression Regulation, Enzymologic - drug effects</topic><topic>Inducible nitric oxide synthase</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Macrophages - enzymology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - genetics</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Nuclear transcription factor-kappa B</topic><topic>Pharmacology. Drug treatments</topic><topic>Receptors, Drug - antagonists & inhibitors</topic><topic>RNA, Messenger - analysis</topic><topic>vanilloid receptors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oh, Gi-Su</creatorcontrib><creatorcontrib>Pae, Hyun-Ock</creatorcontrib><creatorcontrib>Seo, Won-Gil</creatorcontrib><creatorcontrib>Kim, Na-Young</creatorcontrib><creatorcontrib>Pyun, Kwang Ho</creatorcontrib><creatorcontrib>Kim, Il-Kwang</creatorcontrib><creatorcontrib>Shin, Min-kyo</creatorcontrib><creatorcontrib>Chung, Hun-Taeg</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International immunopharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oh, Gi-Su</au><au>Pae, Hyun-Ock</au><au>Seo, Won-Gil</au><au>Kim, Na-Young</au><au>Pyun, Kwang Ho</au><au>Kim, Il-Kwang</au><au>Shin, Min-kyo</au><au>Chung, Hun-Taeg</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Capsazepine, a vanilloid receptor antagonist, inhibits the expression of inducible nitric oxide synthase gene in lipopolysaccharide-stimulated RAW264.7 macrophages through the inactivation of nuclear transcription factor-kappa B</atitle><jtitle>International immunopharmacology</jtitle><addtitle>Int Immunopharmacol</addtitle><date>2001-04</date><risdate>2001</risdate><volume>1</volume><issue>4</issue><spage>777</spage><epage>784</epage><pages>777-784</pages><issn>1567-5769</issn><eissn>1878-1705</eissn><abstract>High amounts of nitric oxide (NO) production following the induction of inducible NO synthase (iNOS) gene expression has been implicated in the pathogenesis of inflammatory diseases. Capsaicin, a vanilloid receptor agonist, is known to have an inhibitory effect on NO production in macrophages. In the present study, we have found that capsazepine (CAPZ), a vanilloid receptor antagonist, also inhibited NO and iNOS protein syntheses induced by lipopolysaccharide in RAW264.7 macrophages via the suppression of iNOS mRNA. The mechanistic studies showed that CAPZ inhibited the expression of iNOS mRNA through the inactivation of nuclear transcription factor-kappa B (NF-κ B). Thus, capsazepine may be a useful candidate for the development of a drug to treat inflammatory diseases related to iNOS gene overexpression.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>11357890</pmid><doi>10.1016/S1567-5769(01)00012-1</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Bones, joints and connective tissue. Antiinflammatory agents Capsaicin Capsaicin - analogs & derivatives Capsaicin - pharmacology Capsazepine Cell Line Gene Expression Regulation, Enzymologic - drug effects Inducible nitric oxide synthase Lipopolysaccharides - pharmacology Macrophages - enzymology Medical sciences Mice NF-kappa B - antagonists & inhibitors Nitric oxide Nitric Oxide - biosynthesis Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - genetics Nitric Oxide Synthase Type II Nuclear transcription factor-kappa B Pharmacology. Drug treatments Receptors, Drug - antagonists & inhibitors RNA, Messenger - analysis vanilloid receptors |
| title | Capsazepine, a vanilloid receptor antagonist, inhibits the expression of inducible nitric oxide synthase gene in lipopolysaccharide-stimulated RAW264.7 macrophages through the inactivation of nuclear transcription factor-kappa B |
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