An inhibitor of inducible nitric oxide synthase ameliorates experimental autoimmune myocarditis in Lewis rats
We studied the effect of nitric oxide (NO) on experimental autoimmune myocarditis (EAC) in rats. We examined the role of inducible nitric oxide synthase (iNOS), an enzyme that produces NO, on hearts affected with EAC, by testing the effects of aminoguanidine (AG), a selective iNOS inhibitor, on the...
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| Veröffentlicht in: | Journal of neuroimmunology 1998-12, Vol.92 (1), p.133-138 |
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| container_title | Journal of neuroimmunology |
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| creator | Shin, Taekyun Tanuma, Naoyuki Kim, Seungjoon Jin, Jaekwang Moon, Changjong Kim, Kiok Kohyama, Kuniko Matsumoto, Yoh Hyun, Byunghwa |
| description | We studied the effect of nitric oxide (NO) on experimental autoimmune myocarditis (EAC) in rats. We examined the role of inducible nitric oxide synthase (iNOS), an enzyme that produces NO, on hearts affected with EAC, by testing the effects of aminoguanidine (AG), a selective iNOS inhibitor, on the course of EAC. Western blotting detected iNOS in the affected cardiac tissues, but not in CFA immunized cases. Immunohistochemically, the majority of ED1
+ macrophages in the EAC lesions were positive for iNOS and nitrotyrosine. A high dose of AG (200 mg/kg/day) significantly reduced the incidence of EAC (
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| doi_str_mv | 10.1016/S0165-5728(98)00194-5 |
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+ macrophages in the EAC lesions were positive for iNOS and nitrotyrosine. A high dose of AG (200 mg/kg/day) significantly reduced the incidence of EAC (
p<0.05) and ameliorated the histological score for the cardiac inflammation (
p<0.01) compared with the low dose AG (100 mg/kg/day) and vehicle treated groups. The immunoblot analysis showed that a high dose of AG effectively suppressed iNOS in hearts affected with EAC. An iNOS band was barely detected in the high dose AG (200 mg/kg) treated group, while it was distinctively visualized in the vehicle and low dose AG (100 mg/kg) treated groups. These results suggest that iNOS is upregulated in EAC lesions and increased NO production plays an important role in the development of EAC. In addition, selective iNOS inhibitors may have a therapeutic role in treating certain autoimmune diseases including EAC.</description><identifier>ISSN: 0165-5728</identifier><identifier>EISSN: 1872-8421</identifier><identifier>DOI: 10.1016/S0165-5728(98)00194-5</identifier><identifier>PMID: 9916888</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Aminoguanidine ; Animals ; Autoimmune Diseases - enzymology ; Autoimmune Diseases - pathology ; Autoimmune Diseases - prevention & control ; Dose-Response Relationship, Drug ; Enzyme Inhibitors - pharmacology ; Experimental autoimmune myocarditis ; Guanidines - pharmacology ; Myocarditis - enzymology ; Myocarditis - pathology ; Myocarditis - prevention & control ; Myocardium - enzymology ; Myocardium - metabolism ; Myocardium - pathology ; Nitric oxide synthase ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Rats ; Rats, Inbred Lew ; Tyrosine - analogs & derivatives ; Tyrosine - metabolism</subject><ispartof>Journal of neuroimmunology, 1998-12, Vol.92 (1), p.133-138</ispartof><rights>1998 Elsevier Science B.V.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c457t-87839fd5558275d0d18bc25cfe951c81a454a62629ef7629976ee89ace0a0663</citedby><cites>FETCH-LOGICAL-c457t-87839fd5558275d0d18bc25cfe951c81a454a62629ef7629976ee89ace0a0663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0165-5728(98)00194-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9916888$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shin, Taekyun</creatorcontrib><creatorcontrib>Tanuma, Naoyuki</creatorcontrib><creatorcontrib>Kim, Seungjoon</creatorcontrib><creatorcontrib>Jin, Jaekwang</creatorcontrib><creatorcontrib>Moon, Changjong</creatorcontrib><creatorcontrib>Kim, Kiok</creatorcontrib><creatorcontrib>Kohyama, Kuniko</creatorcontrib><creatorcontrib>Matsumoto, Yoh</creatorcontrib><creatorcontrib>Hyun, Byunghwa</creatorcontrib><title>An inhibitor of inducible nitric oxide synthase ameliorates experimental autoimmune myocarditis in Lewis rats</title><title>Journal of neuroimmunology</title><addtitle>J Neuroimmunol</addtitle><description>We studied the effect of nitric oxide (NO) on experimental autoimmune myocarditis (EAC) in rats. We examined the role of inducible nitric oxide synthase (iNOS), an enzyme that produces NO, on hearts affected with EAC, by testing the effects of aminoguanidine (AG), a selective iNOS inhibitor, on the course of EAC. Western blotting detected iNOS in the affected cardiac tissues, but not in CFA immunized cases. Immunohistochemically, the majority of ED1
+ macrophages in the EAC lesions were positive for iNOS and nitrotyrosine. A high dose of AG (200 mg/kg/day) significantly reduced the incidence of EAC (
p<0.05) and ameliorated the histological score for the cardiac inflammation (
p<0.01) compared with the low dose AG (100 mg/kg/day) and vehicle treated groups. The immunoblot analysis showed that a high dose of AG effectively suppressed iNOS in hearts affected with EAC. An iNOS band was barely detected in the high dose AG (200 mg/kg) treated group, while it was distinctively visualized in the vehicle and low dose AG (100 mg/kg) treated groups. These results suggest that iNOS is upregulated in EAC lesions and increased NO production plays an important role in the development of EAC. In addition, selective iNOS inhibitors may have a therapeutic role in treating certain autoimmune diseases including EAC.</description><subject>Aminoguanidine</subject><subject>Animals</subject><subject>Autoimmune Diseases - enzymology</subject><subject>Autoimmune Diseases - pathology</subject><subject>Autoimmune Diseases - prevention & control</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Experimental autoimmune myocarditis</subject><subject>Guanidines - pharmacology</subject><subject>Myocarditis - enzymology</subject><subject>Myocarditis - pathology</subject><subject>Myocarditis - prevention & control</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>Nitric oxide synthase</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - metabolism</subject><issn>0165-5728</issn><issn>1872-8421</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUctOwzAQtBAISuETKvmE4BCI0zixTwhVvKRKHOjdcu2NuiiJi-1A-_eYtuLKZXetnZmVZwiZsPyW5ay6e0-FZ7wuxLUUN3nOZJnxIzJioi4yURbsmIz-IGfkPISPBOLTUp6SUylZJYQYke6hp9ivcInReeqa9LCDwWULtMfo0VC3QQs0bPu40gGo7qBF53WEQGGzBo8d9FG3VA_RYdcNPdBu64z2FiOGpEfn8J2GRAkX5KTRbYDLQx-TxdPjYvaSzd-eX2cP88yUvI6ZqMVUNpZzLoqa29wysTQFNw1IzoxguuSlroqqkNDUqcq6AhBSG8h1XlXTMbnay669-xwgRNVhMNC2ugc3BFVJlhTK8l8gq1khBJsmIN8DjXcheGjUOn1c-61iufqNQ-3iUL9eKynULg7FE29yODAsO7B_rIP_aX-_30Ny4wvBq2AQegMWPZiorMN_LvwAWJ-bxQ</recordid><startdate>19981201</startdate><enddate>19981201</enddate><creator>Shin, Taekyun</creator><creator>Tanuma, Naoyuki</creator><creator>Kim, Seungjoon</creator><creator>Jin, Jaekwang</creator><creator>Moon, Changjong</creator><creator>Kim, Kiok</creator><creator>Kohyama, Kuniko</creator><creator>Matsumoto, Yoh</creator><creator>Hyun, Byunghwa</creator><general>Elsevier B.V</general><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>7TK</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19981201</creationdate><title>An inhibitor of inducible nitric oxide synthase ameliorates experimental autoimmune myocarditis in Lewis rats</title><author>Shin, Taekyun ; Tanuma, Naoyuki ; Kim, Seungjoon ; Jin, Jaekwang ; Moon, Changjong ; Kim, Kiok ; Kohyama, Kuniko ; Matsumoto, Yoh ; Hyun, Byunghwa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c457t-87839fd5558275d0d18bc25cfe951c81a454a62629ef7629976ee89ace0a0663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Aminoguanidine</topic><topic>Animals</topic><topic>Autoimmune Diseases - enzymology</topic><topic>Autoimmune Diseases - pathology</topic><topic>Autoimmune Diseases - prevention & control</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Experimental autoimmune myocarditis</topic><topic>Guanidines - pharmacology</topic><topic>Myocarditis - enzymology</topic><topic>Myocarditis - pathology</topic><topic>Myocarditis - prevention & control</topic><topic>Myocardium - enzymology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>Nitric oxide synthase</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shin, Taekyun</creatorcontrib><creatorcontrib>Tanuma, Naoyuki</creatorcontrib><creatorcontrib>Kim, Seungjoon</creatorcontrib><creatorcontrib>Jin, Jaekwang</creatorcontrib><creatorcontrib>Moon, Changjong</creatorcontrib><creatorcontrib>Kim, Kiok</creatorcontrib><creatorcontrib>Kohyama, Kuniko</creatorcontrib><creatorcontrib>Matsumoto, Yoh</creatorcontrib><creatorcontrib>Hyun, Byunghwa</creatorcontrib><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>Neurosciences Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuroimmunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shin, Taekyun</au><au>Tanuma, Naoyuki</au><au>Kim, Seungjoon</au><au>Jin, Jaekwang</au><au>Moon, Changjong</au><au>Kim, Kiok</au><au>Kohyama, Kuniko</au><au>Matsumoto, Yoh</au><au>Hyun, Byunghwa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An inhibitor of inducible nitric oxide synthase ameliorates experimental autoimmune myocarditis in Lewis rats</atitle><jtitle>Journal of neuroimmunology</jtitle><addtitle>J Neuroimmunol</addtitle><date>1998-12-01</date><risdate>1998</risdate><volume>92</volume><issue>1</issue><spage>133</spage><epage>138</epage><pages>133-138</pages><issn>0165-5728</issn><eissn>1872-8421</eissn><abstract>We studied the effect of nitric oxide (NO) on experimental autoimmune myocarditis (EAC) in rats. We examined the role of inducible nitric oxide synthase (iNOS), an enzyme that produces NO, on hearts affected with EAC, by testing the effects of aminoguanidine (AG), a selective iNOS inhibitor, on the course of EAC. Western blotting detected iNOS in the affected cardiac tissues, but not in CFA immunized cases. Immunohistochemically, the majority of ED1
+ macrophages in the EAC lesions were positive for iNOS and nitrotyrosine. A high dose of AG (200 mg/kg/day) significantly reduced the incidence of EAC (
p<0.05) and ameliorated the histological score for the cardiac inflammation (
p<0.01) compared with the low dose AG (100 mg/kg/day) and vehicle treated groups. The immunoblot analysis showed that a high dose of AG effectively suppressed iNOS in hearts affected with EAC. An iNOS band was barely detected in the high dose AG (200 mg/kg) treated group, while it was distinctively visualized in the vehicle and low dose AG (100 mg/kg) treated groups. These results suggest that iNOS is upregulated in EAC lesions and increased NO production plays an important role in the development of EAC. In addition, selective iNOS inhibitors may have a therapeutic role in treating certain autoimmune diseases including EAC.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>9916888</pmid><doi>10.1016/S0165-5728(98)00194-5</doi><tpages>6</tpages></addata></record> |
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| subjects | Aminoguanidine Animals Autoimmune Diseases - enzymology Autoimmune Diseases - pathology Autoimmune Diseases - prevention & control Dose-Response Relationship, Drug Enzyme Inhibitors - pharmacology Experimental autoimmune myocarditis Guanidines - pharmacology Myocarditis - enzymology Myocarditis - pathology Myocarditis - prevention & control Myocardium - enzymology Myocardium - metabolism Myocardium - pathology Nitric oxide synthase Nitric Oxide Synthase - antagonists & inhibitors Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Rats Rats, Inbred Lew Tyrosine - analogs & derivatives Tyrosine - metabolism |
| title | An inhibitor of inducible nitric oxide synthase ameliorates experimental autoimmune myocarditis in Lewis rats |
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