Ischemic postconditioning provides cardioprotective and antiapoptotic effects against ischemia–reperfusion injury through iNOS inhibition in hyperthyroid rats
Ischemic postconditioning (IPost) is a strategy to provide protection against ischemia–reperfusion (IR) injury. The cardioprotective effects of IPost in cases of ischemic heart disease along with co-morbidities like hyperthyroidism remain unknown. The aim of this study was to investigate the effects...
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| Veröffentlicht in: | Gene 2015-10, Vol.570 (2), p.185-190 |
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| creator | Zaman, Jalal Jeddi, Sajad Daneshpour, Maryam Sadat Zarkesh, Maryam Daneshian, Zahra Ghasemi, Asghar |
| description | Ischemic postconditioning (IPost) is a strategy to provide protection against ischemia–reperfusion (IR) injury. The cardioprotective effects of IPost in cases of ischemic heart disease along with co-morbidities like hyperthyroidism remain unknown. The aim of this study was to investigate the effects of IPost on expression of eNOS, iNOS, Bax, and Bcl-2 genes in hyperthyroid male rats, subjected to myocardial IR. Hyperthyroidism was induced by adding thyroxine to drinking water for a period of 21days. Using the Langendorff device hearts were perfused, then subjected to a 30-minute global ischemia which was followed by 120min of reperfusion; subsequently IPost was induced immediately after ischemia. Results indicated that following IR, expression of eNOS and Bcl-2 decreased, whereas expression of iNOS and Bax increased in both the control and hyperthyroid groups. In hyperthyroid animals, IPost significantly increased expression of eNOS by 3.19 fold and Bcl-2 by 3.66 fold; it also decreased expression of Bax by 51%, and reduced IR-induced DNA laddering pattern and infarct size (45.7±1.82% vs. 59.3±1.83%, p |
| doi_str_mv | 10.1016/j.gene.2015.06.011 |
| format | Article |
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•Ischemic postconditioning provides cardioprotection in hyperthyroidism.•Ischemic postconditioning reduced apoptosis in hyperthyroidism.•Ischemic postconditioning changes eNOS, Bcl-2, and Bax expression in hyperthyroidism.</description><identifier>ISSN: 0378-1119</identifier><identifier>EISSN: 1879-0038</identifier><identifier>DOI: 10.1016/j.gene.2015.06.011</identifier><identifier>PMID: 26055090</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; Apoptosis ; Gene expression ; Hyperthyroidism ; Hyperthyroidism - enzymology ; Hyperthyroidism - pathology ; Ischemia ; Ischemic Postconditioning ; Male ; Nitric Oxide Synthase Type II - antagonists & inhibitors ; Postconditioning ; Rats ; Rats, Wistar ; Reperfusion Injury - prevention & control</subject><ispartof>Gene, 2015-10, Vol.570 (2), p.185-190</ispartof><rights>2015 Elsevier B.V.</rights><rights>Copyright © 2015 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-a9f7c81b0f3909a516108941f39043374abb2f6bfd733d03c9db7fc0b0ea2da23</citedby><cites>FETCH-LOGICAL-c389t-a9f7c81b0f3909a516108941f39043374abb2f6bfd733d03c9db7fc0b0ea2da23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0378111915007192$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26055090$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zaman, Jalal</creatorcontrib><creatorcontrib>Jeddi, Sajad</creatorcontrib><creatorcontrib>Daneshpour, Maryam Sadat</creatorcontrib><creatorcontrib>Zarkesh, Maryam</creatorcontrib><creatorcontrib>Daneshian, Zahra</creatorcontrib><creatorcontrib>Ghasemi, Asghar</creatorcontrib><title>Ischemic postconditioning provides cardioprotective and antiapoptotic effects against ischemia–reperfusion injury through iNOS inhibition in hyperthyroid rats</title><title>Gene</title><addtitle>Gene</addtitle><description>Ischemic postconditioning (IPost) is a strategy to provide protection against ischemia–reperfusion (IR) injury. The cardioprotective effects of IPost in cases of ischemic heart disease along with co-morbidities like hyperthyroidism remain unknown. The aim of this study was to investigate the effects of IPost on expression of eNOS, iNOS, Bax, and Bcl-2 genes in hyperthyroid male rats, subjected to myocardial IR. Hyperthyroidism was induced by adding thyroxine to drinking water for a period of 21days. Using the Langendorff device hearts were perfused, then subjected to a 30-minute global ischemia which was followed by 120min of reperfusion; subsequently IPost was induced immediately after ischemia. Results indicated that following IR, expression of eNOS and Bcl-2 decreased, whereas expression of iNOS and Bax increased in both the control and hyperthyroid groups. In hyperthyroid animals, IPost significantly increased expression of eNOS by 3.19 fold and Bcl-2 by 3.66 fold; it also decreased expression of Bax by 51%, and reduced IR-induced DNA laddering pattern and infarct size (45.7±1.82% vs. 59.3±1.83%, p<0.05) in the presence of aminoguanidine (AG), a selective iNOS inhibitor. In conclusion, IPost per se could not provide cardioprotection against myocardial ischemia in hyperthyroid rats, a loss of which however was restored by the combination of IPost and iNOS inhibition that acts by a decrease in Bax and an increase in both eNOS and Bcl-2 expression.
•Ischemic postconditioning provides cardioprotection in hyperthyroidism.•Ischemic postconditioning reduced apoptosis in hyperthyroidism.•Ischemic postconditioning changes eNOS, Bcl-2, and Bax expression in hyperthyroidism.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Gene expression</subject><subject>Hyperthyroidism</subject><subject>Hyperthyroidism - enzymology</subject><subject>Hyperthyroidism - pathology</subject><subject>Ischemia</subject><subject>Ischemic Postconditioning</subject><subject>Male</subject><subject>Nitric Oxide Synthase Type II - antagonists & inhibitors</subject><subject>Postconditioning</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Reperfusion Injury - prevention & control</subject><issn>0378-1119</issn><issn>1879-0038</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcGOFCEQhonRuOPqC3gwHL10WzQ93U3ixWzU3WTjHtQzoaGYZjIDLdCTzM138AV8Np9kGWf1aCQhVMFXP6n6CXnJoGbAujfbeoMe6wbYuoauBsYekRUbelEB8OExWQHvh4oxJi7Is5S2UNZ63TwlF01XAhCwIj9vkp5w7zSdQ8o6eOOyC975DZ1jODiDiWoVjQslzaizOyBV3pSdnZrDnEMuxWhteUtUbZTzKVN3VlW_vv-IOGO0Syqq1PntEo80TzEsm4m6T3efy93kxt-flpBOx0Ln6RiDMzSqnJ6TJ1btEr54OC_J1w_vv1xdV7d3H2-u3t1Wmg8iV0rYXg9sBMsFCLVmHYNBtOyUtpz3rRrHxnajNT3nBrgWZuythhFQNUY1_JK8PuuWPr8tmLLclyZwt1Mew5Ik60GU2bLmv9CWt0PHeEGbM6pjSCmilXN0exWPkoE8mSi38mSiPJkooZPFxFL06kF_Gfdo_pb8ca0Ab88AloEcHEaZtEOv0bhYbJAmuH_p3wNrVrPX</recordid><startdate>20151010</startdate><enddate>20151010</enddate><creator>Zaman, Jalal</creator><creator>Jeddi, Sajad</creator><creator>Daneshpour, Maryam Sadat</creator><creator>Zarkesh, Maryam</creator><creator>Daneshian, Zahra</creator><creator>Ghasemi, Asghar</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>7X8</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20151010</creationdate><title>Ischemic postconditioning provides cardioprotective and antiapoptotic effects against ischemia–reperfusion injury through iNOS inhibition in hyperthyroid rats</title><author>Zaman, Jalal ; Jeddi, Sajad ; Daneshpour, Maryam Sadat ; Zarkesh, Maryam ; Daneshian, Zahra ; Ghasemi, Asghar</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-a9f7c81b0f3909a516108941f39043374abb2f6bfd733d03c9db7fc0b0ea2da23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Gene expression</topic><topic>Hyperthyroidism</topic><topic>Hyperthyroidism - enzymology</topic><topic>Hyperthyroidism - pathology</topic><topic>Ischemia</topic><topic>Ischemic Postconditioning</topic><topic>Male</topic><topic>Nitric Oxide Synthase Type II - antagonists & inhibitors</topic><topic>Postconditioning</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Reperfusion Injury - prevention & control</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zaman, Jalal</creatorcontrib><creatorcontrib>Jeddi, Sajad</creatorcontrib><creatorcontrib>Daneshpour, Maryam Sadat</creatorcontrib><creatorcontrib>Zarkesh, Maryam</creatorcontrib><creatorcontrib>Daneshian, Zahra</creatorcontrib><creatorcontrib>Ghasemi, Asghar</creatorcontrib><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><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Gene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zaman, Jalal</au><au>Jeddi, Sajad</au><au>Daneshpour, Maryam Sadat</au><au>Zarkesh, Maryam</au><au>Daneshian, Zahra</au><au>Ghasemi, Asghar</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ischemic postconditioning provides cardioprotective and antiapoptotic effects against ischemia–reperfusion injury through iNOS inhibition in hyperthyroid rats</atitle><jtitle>Gene</jtitle><addtitle>Gene</addtitle><date>2015-10-10</date><risdate>2015</risdate><volume>570</volume><issue>2</issue><spage>185</spage><epage>190</epage><pages>185-190</pages><issn>0378-1119</issn><eissn>1879-0038</eissn><abstract>Ischemic postconditioning (IPost) is a strategy to provide protection against ischemia–reperfusion (IR) injury. The cardioprotective effects of IPost in cases of ischemic heart disease along with co-morbidities like hyperthyroidism remain unknown. The aim of this study was to investigate the effects of IPost on expression of eNOS, iNOS, Bax, and Bcl-2 genes in hyperthyroid male rats, subjected to myocardial IR. Hyperthyroidism was induced by adding thyroxine to drinking water for a period of 21days. Using the Langendorff device hearts were perfused, then subjected to a 30-minute global ischemia which was followed by 120min of reperfusion; subsequently IPost was induced immediately after ischemia. Results indicated that following IR, expression of eNOS and Bcl-2 decreased, whereas expression of iNOS and Bax increased in both the control and hyperthyroid groups. In hyperthyroid animals, IPost significantly increased expression of eNOS by 3.19 fold and Bcl-2 by 3.66 fold; it also decreased expression of Bax by 51%, and reduced IR-induced DNA laddering pattern and infarct size (45.7±1.82% vs. 59.3±1.83%, p<0.05) in the presence of aminoguanidine (AG), a selective iNOS inhibitor. In conclusion, IPost per se could not provide cardioprotection against myocardial ischemia in hyperthyroid rats, a loss of which however was restored by the combination of IPost and iNOS inhibition that acts by a decrease in Bax and an increase in both eNOS and Bcl-2 expression.
•Ischemic postconditioning provides cardioprotection in hyperthyroidism.•Ischemic postconditioning reduced apoptosis in hyperthyroidism.•Ischemic postconditioning changes eNOS, Bcl-2, and Bax expression in hyperthyroidism.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>26055090</pmid><doi>10.1016/j.gene.2015.06.011</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Apoptosis Gene expression Hyperthyroidism Hyperthyroidism - enzymology Hyperthyroidism - pathology Ischemia Ischemic Postconditioning Male Nitric Oxide Synthase Type II - antagonists & inhibitors Postconditioning Rats Rats, Wistar Reperfusion Injury - prevention & control |
| title | Ischemic postconditioning provides cardioprotective and antiapoptotic effects against ischemia–reperfusion injury through iNOS inhibition in hyperthyroid rats |
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