Ghrelin inhibits post-infarct myocardial remodeling and improves cardiac function through anti-inflammation effect
Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial cardiac effects on chronic heart failure (CHF) recently. In this study, we attempted to investigate the mechanisms for the effect of ghrelin on ventricular remodeling following acute myocardial infarction (...
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| Veröffentlicht in: | Peptides (New York, N.Y. : 1980) N.Y. : 1980), 2009-12, Vol.30 (12), p.2286-2291 |
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| creator | Huang, Cong-Xin Yuan, Ming-Jie Huang, He Wu, Gang Liu, Yu Yu, Sheng-Bo Li, Hai-Tao Wang, Tao |
| description | Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial cardiac effects on chronic heart failure (CHF) recently. In this study, we attempted to investigate the mechanisms for the effect of ghrelin on ventricular remodeling following acute myocardial infarction (MI). Ligation of a coronary artery was used to create an MI in rats. One week after MI, ghrelin (100
μg/kg) or saline was injected subcutaneously twice a day for 4 weeks. When compared to sham groups, ghrelin administration significantly decreased left ventricular (LV) remodeling in post-MI rats, as indicated by increased LV maximum rate of pressure, LV fractional shortening and scar thickness; and decreased LV end-diastolic pressure, LV end-systolic diameter, LV end-diastolic diameter and cardiocytocytes apoptosis. Moreover, ghrelin inhibited the inflammatory response, as shown by decreased mRNA and protein levels of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α). Subsequently, the expression of matrix metalloproteinase (MMP)-2 and MMP-9 were also inhibited by ghrelin injection. Ghrelin alleviates LV dysfunction and ventricular remodeling in post-MI rats. This suggests that the beneficial effects of ghrelin on CHF may result from an inhibition of the inflammatory response. |
| doi_str_mv | 10.1016/j.peptides.2009.09.004 |
| format | Article |
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μg/kg) or saline was injected subcutaneously twice a day for 4 weeks. When compared to sham groups, ghrelin administration significantly decreased left ventricular (LV) remodeling in post-MI rats, as indicated by increased LV maximum rate of pressure, LV fractional shortening and scar thickness; and decreased LV end-diastolic pressure, LV end-systolic diameter, LV end-diastolic diameter and cardiocytocytes apoptosis. Moreover, ghrelin inhibited the inflammatory response, as shown by decreased mRNA and protein levels of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α). Subsequently, the expression of matrix metalloproteinase (MMP)-2 and MMP-9 were also inhibited by ghrelin injection. Ghrelin alleviates LV dysfunction and ventricular remodeling in post-MI rats. This suggests that the beneficial effects of ghrelin on CHF may result from an inhibition of the inflammatory response.</description><identifier>ISSN: 0196-9781</identifier><identifier>EISSN: 1873-5169</identifier><identifier>DOI: 10.1016/j.peptides.2009.09.004</identifier><identifier>PMID: 19747956</identifier><identifier>CODEN: PPTDD5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Anti-Inflammatory Agents - pharmacology ; Biological and medical sciences ; Blotting, Western ; Cardiology. Vascular system ; Coronary heart disease ; Enzyme-Linked Immunosorbent Assay ; Fundamental and applied biological sciences. Psychology ; Ghrelin ; Ghrelin - pharmacology ; Heart ; In Situ Nick-End Labeling ; Interleukin-1beta - genetics ; Interleukin-1beta - metabolism ; Male ; Matrix metalloproteinase ; Matrix Metalloproteinase 2 - genetics ; Matrix Metalloproteinase 2 - metabolism ; Matrix Metalloproteinase 9 - genetics ; Matrix Metalloproteinase 9 - metabolism ; Medical sciences ; Myocardial infarction ; Myocardial Infarction - immunology ; Myocarditis. Cardiomyopathies ; Polymerase Chain Reaction ; Pro-inflammatory cytokines ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Ventricular Remodeling - drug effects ; Vertebrates: endocrinology</subject><ispartof>Peptides (New York, N.Y. : 1980), 2009-12, Vol.30 (12), p.2286-2291</ispartof><rights>2009 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-ee773171bc93e24ab304f6dacebb1ffe202fcca9bc3731c2cceab39cf410e5ad3</citedby><cites>FETCH-LOGICAL-c463t-ee773171bc93e24ab304f6dacebb1ffe202fcca9bc3731c2cceab39cf410e5ad3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.peptides.2009.09.004$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22264403$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19747956$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Cong-Xin</creatorcontrib><creatorcontrib>Yuan, Ming-Jie</creatorcontrib><creatorcontrib>Huang, He</creatorcontrib><creatorcontrib>Wu, Gang</creatorcontrib><creatorcontrib>Liu, Yu</creatorcontrib><creatorcontrib>Yu, Sheng-Bo</creatorcontrib><creatorcontrib>Li, Hai-Tao</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><title>Ghrelin inhibits post-infarct myocardial remodeling and improves cardiac function through anti-inflammation effect</title><title>Peptides (New York, N.Y. : 1980)</title><addtitle>Peptides</addtitle><description>Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial cardiac effects on chronic heart failure (CHF) recently. In this study, we attempted to investigate the mechanisms for the effect of ghrelin on ventricular remodeling following acute myocardial infarction (MI). Ligation of a coronary artery was used to create an MI in rats. One week after MI, ghrelin (100
μg/kg) or saline was injected subcutaneously twice a day for 4 weeks. When compared to sham groups, ghrelin administration significantly decreased left ventricular (LV) remodeling in post-MI rats, as indicated by increased LV maximum rate of pressure, LV fractional shortening and scar thickness; and decreased LV end-diastolic pressure, LV end-systolic diameter, LV end-diastolic diameter and cardiocytocytes apoptosis. Moreover, ghrelin inhibited the inflammatory response, as shown by decreased mRNA and protein levels of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α). Subsequently, the expression of matrix metalloproteinase (MMP)-2 and MMP-9 were also inhibited by ghrelin injection. Ghrelin alleviates LV dysfunction and ventricular remodeling in post-MI rats. This suggests that the beneficial effects of ghrelin on CHF may result from an inhibition of the inflammatory response.</description><subject>Animals</subject><subject>Anti-Inflammatory Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cardiology. Vascular system</subject><subject>Coronary heart disease</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Ghrelin</subject><subject>Ghrelin - pharmacology</subject><subject>Heart</subject><subject>In Situ Nick-End Labeling</subject><subject>Interleukin-1beta - genetics</subject><subject>Interleukin-1beta - metabolism</subject><subject>Male</subject><subject>Matrix metalloproteinase</subject><subject>Matrix Metalloproteinase 2 - genetics</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Matrix Metalloproteinase 9 - genetics</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medical sciences</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - immunology</subject><subject>Myocarditis. Cardiomyopathies</subject><subject>Polymerase Chain Reaction</subject><subject>Pro-inflammatory cytokines</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Ventricular Remodeling - drug effects</subject><subject>Vertebrates: endocrinology</subject><issn>0196-9781</issn><issn>1873-5169</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0MFu1DAQBmALgehSeIXKF8Qpix07zvoGqqAgVeICZ8sZj7teJU6wnUp9exx2gSPSSD7MN-PRT8gNZ3vOuHp_2i-4lOAw71vG9H4rJp-RHT_0oum40s_JjnGtGt0f-BV5lfOJVSH14SW54rqXve7UjqS7Y8IxRBriMQyhZLrMuTQhepug0OlpBptcsCNNOM1uow_URkfDtKT5ETM994H6NUIJc6TlmOb14VhVCdui0U6T_d1B7xHKa_LC2zHjm8t7TX58_vT99ktz_-3u6-3H-wakEqVB7HvBez6AFthKOwgmvXIWcBh4XdSy1gNYPYCoDloArEaDl5xhZ524Ju_Oe-uhP1fMxUwhA46jjTiv2fRC8q5jTFWpzhLSnHNCb5YUJpueDGdmi9uczJ-4zRa32YrJOnhz-WIdJnT_xi75VvD2AmwGO_pkI4T817Vtq6RkoroPZ4c1kMeAyWQIGAFdSDUy4-bwv1t-ARdEpjE</recordid><startdate>20091201</startdate><enddate>20091201</enddate><creator>Huang, Cong-Xin</creator><creator>Yuan, Ming-Jie</creator><creator>Huang, He</creator><creator>Wu, Gang</creator><creator>Liu, Yu</creator><creator>Yu, Sheng-Bo</creator><creator>Li, Hai-Tao</creator><creator>Wang, Tao</creator><general>Elsevier Inc</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>20091201</creationdate><title>Ghrelin inhibits post-infarct myocardial remodeling and improves cardiac function through anti-inflammation effect</title><author>Huang, Cong-Xin ; Yuan, Ming-Jie ; Huang, He ; Wu, Gang ; Liu, Yu ; Yu, Sheng-Bo ; Li, Hai-Tao ; Wang, Tao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-ee773171bc93e24ab304f6dacebb1ffe202fcca9bc3731c2cceab39cf410e5ad3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Anti-Inflammatory Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cardiology. Vascular system</topic><topic>Coronary heart disease</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Ghrelin</topic><topic>Ghrelin - pharmacology</topic><topic>Heart</topic><topic>In Situ Nick-End Labeling</topic><topic>Interleukin-1beta - genetics</topic><topic>Interleukin-1beta - metabolism</topic><topic>Male</topic><topic>Matrix metalloproteinase</topic><topic>Matrix Metalloproteinase 2 - genetics</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Matrix Metalloproteinase 9 - genetics</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medical sciences</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - immunology</topic><topic>Myocarditis. Cardiomyopathies</topic><topic>Polymerase Chain Reaction</topic><topic>Pro-inflammatory cytokines</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Ventricular Remodeling - drug effects</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Cong-Xin</creatorcontrib><creatorcontrib>Yuan, Ming-Jie</creatorcontrib><creatorcontrib>Huang, He</creatorcontrib><creatorcontrib>Wu, Gang</creatorcontrib><creatorcontrib>Liu, Yu</creatorcontrib><creatorcontrib>Yu, Sheng-Bo</creatorcontrib><creatorcontrib>Li, Hai-Tao</creatorcontrib><creatorcontrib>Wang, Tao</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>Peptides (New York, N.Y. : 1980)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Cong-Xin</au><au>Yuan, Ming-Jie</au><au>Huang, He</au><au>Wu, Gang</au><au>Liu, Yu</au><au>Yu, Sheng-Bo</au><au>Li, Hai-Tao</au><au>Wang, Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ghrelin inhibits post-infarct myocardial remodeling and improves cardiac function through anti-inflammation effect</atitle><jtitle>Peptides (New York, N.Y. : 1980)</jtitle><addtitle>Peptides</addtitle><date>2009-12-01</date><risdate>2009</risdate><volume>30</volume><issue>12</issue><spage>2286</spage><epage>2291</epage><pages>2286-2291</pages><issn>0196-9781</issn><eissn>1873-5169</eissn><coden>PPTDD5</coden><abstract>Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial cardiac effects on chronic heart failure (CHF) recently. In this study, we attempted to investigate the mechanisms for the effect of ghrelin on ventricular remodeling following acute myocardial infarction (MI). Ligation of a coronary artery was used to create an MI in rats. One week after MI, ghrelin (100
μg/kg) or saline was injected subcutaneously twice a day for 4 weeks. When compared to sham groups, ghrelin administration significantly decreased left ventricular (LV) remodeling in post-MI rats, as indicated by increased LV maximum rate of pressure, LV fractional shortening and scar thickness; and decreased LV end-diastolic pressure, LV end-systolic diameter, LV end-diastolic diameter and cardiocytocytes apoptosis. Moreover, ghrelin inhibited the inflammatory response, as shown by decreased mRNA and protein levels of interleukin (IL)-1β and tumor necrosis factor-α (TNF-α). Subsequently, the expression of matrix metalloproteinase (MMP)-2 and MMP-9 were also inhibited by ghrelin injection. Ghrelin alleviates LV dysfunction and ventricular remodeling in post-MI rats. This suggests that the beneficial effects of ghrelin on CHF may result from an inhibition of the inflammatory response.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>19747956</pmid><doi>10.1016/j.peptides.2009.09.004</doi><tpages>6</tpages></addata></record> |
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| ispartof | Peptides (New York, N.Y. : 1980), 2009-12, Vol.30 (12), p.2286-2291 |
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| subjects | Animals Anti-Inflammatory Agents - pharmacology Biological and medical sciences Blotting, Western Cardiology. Vascular system Coronary heart disease Enzyme-Linked Immunosorbent Assay Fundamental and applied biological sciences. Psychology Ghrelin Ghrelin - pharmacology Heart In Situ Nick-End Labeling Interleukin-1beta - genetics Interleukin-1beta - metabolism Male Matrix metalloproteinase Matrix Metalloproteinase 2 - genetics Matrix Metalloproteinase 2 - metabolism Matrix Metalloproteinase 9 - genetics Matrix Metalloproteinase 9 - metabolism Medical sciences Myocardial infarction Myocardial Infarction - immunology Myocarditis. Cardiomyopathies Polymerase Chain Reaction Pro-inflammatory cytokines Rats Rats, Sprague-Dawley Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Ventricular Remodeling - drug effects Vertebrates: endocrinology |
| title | Ghrelin inhibits post-infarct myocardial remodeling and improves cardiac function through anti-inflammation effect |
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