Chrysin attenuates interstitial fibrosis and improves cardiac function in a rat model of acute myocardial infarction
Interstitial fibrosis after acute myocardial infarction (MI) leads to cardiac structural remodeling and dysfunction. The peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist chrysin has been shown to protect injured myocardium through suppression of oxidative stress and inflammation. Th...
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| Veröffentlicht in: | Journal of molecular histology 2018-12, Vol.49 (6), p.555-565 |
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| creator | Yang, Mei Xiong, Jun Zou, Qiang Wang, Dan-Dan Huang, Cong-Xin |
| description | Interstitial fibrosis after acute myocardial infarction (MI) leads to cardiac structural remodeling and dysfunction. The peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist chrysin has been shown to protect injured myocardium through suppression of oxidative stress and inflammation. This study was designed to investigate the effect and mechanism of chrysin on myocardial fibrosis. A rat MI model was created by ligating the left coronary artery. The rats with MI were treated with chrysin (40 mg/kg/day) or 0.5% carboxymethylcellulose sodium by intragastric administration for 4 weeks after operation. The effect of chrysin on cardiac fibroblasts (CFs) were also assessed in vitro. Echocardiography showed that cardiac function was significantly improved after chrysin treatment. Chrysin reduced the levels of MDA and SOD and GSH-Px in myocardial tissue. Chrysin attenuated the interstitial and perivascular fibrosis and the expression of collagenlin the peri-infarcted zone and remarkably decreased the levels of matrix metalloproteinase-2 (MMP-2) and MMP-9. Chrysin up-regulated PPAR-γ and inhibited the nuclear factor-kappa B (NF-κB) pathway by suppressing inhibitor kappa B kinase β phosphorylation. Immunohistochemistry analysis and PCR detected downregulated expression of AP-1 after chrysin treatment. Chrysin also markedly reduced the increased α-SMA, typeland type III collagen expression of CFs mediated by AngII in vitro. In conclusion, chrysin has an antifibrosis cardioprotective effect on the infarct peripheral zone after MI. The underlined mechanism may be the up-regulation of PPAR-γ and inhibition of the NF-κB and AP1 pathway. |
| doi_str_mv | 10.1007/s10735-018-9793-0 |
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The peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist chrysin has been shown to protect injured myocardium through suppression of oxidative stress and inflammation. This study was designed to investigate the effect and mechanism of chrysin on myocardial fibrosis. A rat MI model was created by ligating the left coronary artery. The rats with MI were treated with chrysin (40 mg/kg/day) or 0.5% carboxymethylcellulose sodium by intragastric administration for 4 weeks after operation. The effect of chrysin on cardiac fibroblasts (CFs) were also assessed in vitro. Echocardiography showed that cardiac function was significantly improved after chrysin treatment. Chrysin reduced the levels of MDA and SOD and GSH-Px in myocardial tissue. Chrysin attenuated the interstitial and perivascular fibrosis and the expression of collagenlin the peri-infarcted zone and remarkably decreased the levels of matrix metalloproteinase-2 (MMP-2) and MMP-9. Chrysin up-regulated PPAR-γ and inhibited the nuclear factor-kappa B (NF-κB) pathway by suppressing inhibitor kappa B kinase β phosphorylation. Immunohistochemistry analysis and PCR detected downregulated expression of AP-1 after chrysin treatment. Chrysin also markedly reduced the increased α-SMA, typeland type III collagen expression of CFs mediated by AngII in vitro. In conclusion, chrysin has an antifibrosis cardioprotective effect on the infarct peripheral zone after MI. The underlined mechanism may be the up-regulation of PPAR-γ and inhibition of the NF-κB and AP1 pathway.</description><identifier>ISSN: 1567-2379</identifier><identifier>EISSN: 1567-2387</identifier><identifier>DOI: 10.1007/s10735-018-9793-0</identifier><identifier>PMID: 30225683</identifier><language>eng</language><publisher>Dordrecht: Springer Netherlands</publisher><subject>Angiotensin II ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Carboxymethylcellulose ; Cardiac function ; Cell Biology ; Collagen (type III) ; Coronary artery ; Developmental Biology ; Disease Models, Animal ; Echocardiography ; Enzyme inhibitors ; Fibroblasts ; Fibroblasts - drug effects ; Fibrosis ; Fibrosis - drug therapy ; Flavonoids - pharmacology ; Flavonoids - therapeutic use ; Gelatinase A ; Gelatinase B ; Heart - physiopathology ; Heart attacks ; Immunohistochemistry ; Life Sciences ; Matrix metalloproteinase ; Metalloproteinase ; Myocardial infarction ; Myocardial Infarction - drug therapy ; Myocardial Infarction - pathology ; Myocardial Infarction - physiopathology ; Myocardium ; NF-kappa B - antagonists & inhibitors ; NF-κB protein ; Original Paper ; Oxidative stress ; Peroxisome proliferator-activated receptors ; Phosphorylation ; PPAR gamma - agonists ; PPAR gamma - genetics ; Rats ; Rodents ; Sodium ; Transcription Factor AP-1 - antagonists & inhibitors ; Transcription Factor AP-1 - metabolism ; Transcription factors ; Up-Regulation - drug effects</subject><ispartof>Journal of molecular histology, 2018-12, Vol.49 (6), p.555-565</ispartof><rights>Springer Nature B.V. 2018</rights><rights>Journal of Molecular Histology is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-60799e949b8d03e313405530a2f8ff9857ecf7169b8e5128270d7dc73a4fbef53</citedby><cites>FETCH-LOGICAL-c372t-60799e949b8d03e313405530a2f8ff9857ecf7169b8e5128270d7dc73a4fbef53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10735-018-9793-0$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10735-018-9793-0$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30225683$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yang, Mei</creatorcontrib><creatorcontrib>Xiong, Jun</creatorcontrib><creatorcontrib>Zou, Qiang</creatorcontrib><creatorcontrib>Wang, Dan-Dan</creatorcontrib><creatorcontrib>Huang, Cong-Xin</creatorcontrib><title>Chrysin attenuates interstitial fibrosis and improves cardiac function in a rat model of acute myocardial infarction</title><title>Journal of molecular histology</title><addtitle>J Mol Hist</addtitle><addtitle>J Mol Histol</addtitle><description>Interstitial fibrosis after acute myocardial infarction (MI) leads to cardiac structural remodeling and dysfunction. The peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist chrysin has been shown to protect injured myocardium through suppression of oxidative stress and inflammation. This study was designed to investigate the effect and mechanism of chrysin on myocardial fibrosis. A rat MI model was created by ligating the left coronary artery. The rats with MI were treated with chrysin (40 mg/kg/day) or 0.5% carboxymethylcellulose sodium by intragastric administration for 4 weeks after operation. The effect of chrysin on cardiac fibroblasts (CFs) were also assessed in vitro. Echocardiography showed that cardiac function was significantly improved after chrysin treatment. Chrysin reduced the levels of MDA and SOD and GSH-Px in myocardial tissue. Chrysin attenuated the interstitial and perivascular fibrosis and the expression of collagenlin the peri-infarcted zone and remarkably decreased the levels of matrix metalloproteinase-2 (MMP-2) and MMP-9. Chrysin up-regulated PPAR-γ and inhibited the nuclear factor-kappa B (NF-κB) pathway by suppressing inhibitor kappa B kinase β phosphorylation. Immunohistochemistry analysis and PCR detected downregulated expression of AP-1 after chrysin treatment. Chrysin also markedly reduced the increased α-SMA, typeland type III collagen expression of CFs mediated by AngII in vitro. In conclusion, chrysin has an antifibrosis cardioprotective effect on the infarct peripheral zone after MI. The underlined mechanism may be the up-regulation of PPAR-γ and inhibition of the NF-κB and AP1 pathway.</description><subject>Angiotensin II</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Carboxymethylcellulose</subject><subject>Cardiac function</subject><subject>Cell Biology</subject><subject>Collagen (type III)</subject><subject>Coronary artery</subject><subject>Developmental Biology</subject><subject>Disease Models, Animal</subject><subject>Echocardiography</subject><subject>Enzyme inhibitors</subject><subject>Fibroblasts</subject><subject>Fibroblasts - drug effects</subject><subject>Fibrosis</subject><subject>Fibrosis - drug therapy</subject><subject>Flavonoids - pharmacology</subject><subject>Flavonoids - therapeutic use</subject><subject>Gelatinase A</subject><subject>Gelatinase B</subject><subject>Heart - physiopathology</subject><subject>Heart attacks</subject><subject>Immunohistochemistry</subject><subject>Life Sciences</subject><subject>Matrix metalloproteinase</subject><subject>Metalloproteinase</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Myocardium</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-κB protein</subject><subject>Original Paper</subject><subject>Oxidative stress</subject><subject>Peroxisome proliferator-activated receptors</subject><subject>Phosphorylation</subject><subject>PPAR gamma - agonists</subject><subject>PPAR gamma - genetics</subject><subject>Rats</subject><subject>Rodents</subject><subject>Sodium</subject><subject>Transcription Factor AP-1 - antagonists & inhibitors</subject><subject>Transcription Factor AP-1 - metabolism</subject><subject>Transcription factors</subject><subject>Up-Regulation - drug effects</subject><issn>1567-2379</issn><issn>1567-2387</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kUFLHTEQx0OpVH32A_RSAr30sjpJ3m6SY3loFQQveg552Ukb2c3aJCu8b2-eqxYETxmY3_wzzI-QbwxOGYA8ywykaBtgqtFSiwY-kSPWdrLhQsnPb7XUh-Q453sArrq1_kIOBXDedkockbL5m3Y5RGpLwTjbgpmGWDDlEkqwA_Vhm6YcMrWxp2F8SNNjRZxNfbCO-jm6EqZI9wk02ULHqceBTp5aNxek425a2KEi3qZn-oQceDtk_Pryrsjdxfnt5rK5vvl9tfl13TgheWk6kFqjXuut6kGgYGINbSvAcq-816qV6LxkXe1jy7jiEnrZOyns2m_Rt2JFfi65det_M-ZixpAdDoONOM3ZcAZacKWEqOiPd-j9NKdYt9tTCriW9dYrwhbK1ZvkhN48pDDatDMMzF6JWZSYqsTslRioM99fkuftiP3bxKuDCvAFyLUV_2D6__XHqU-0upeL</recordid><startdate>20181201</startdate><enddate>20181201</enddate><creator>Yang, Mei</creator><creator>Xiong, Jun</creator><creator>Zou, Qiang</creator><creator>Wang, Dan-Dan</creator><creator>Huang, Cong-Xin</creator><general>Springer Netherlands</general><general>Springer Nature 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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20181201</creationdate><title>Chrysin attenuates interstitial fibrosis and improves cardiac function in a rat model of acute myocardial infarction</title><author>Yang, Mei ; Xiong, Jun ; Zou, Qiang ; Wang, Dan-Dan ; Huang, Cong-Xin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-60799e949b8d03e313405530a2f8ff9857ecf7169b8e5128270d7dc73a4fbef53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Angiotensin II</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Carboxymethylcellulose</topic><topic>Cardiac function</topic><topic>Cell Biology</topic><topic>Collagen (type III)</topic><topic>Coronary artery</topic><topic>Developmental Biology</topic><topic>Disease Models, Animal</topic><topic>Echocardiography</topic><topic>Enzyme inhibitors</topic><topic>Fibroblasts</topic><topic>Fibroblasts - drug effects</topic><topic>Fibrosis</topic><topic>Fibrosis - drug therapy</topic><topic>Flavonoids - pharmacology</topic><topic>Flavonoids - therapeutic use</topic><topic>Gelatinase A</topic><topic>Gelatinase B</topic><topic>Heart - physiopathology</topic><topic>Heart attacks</topic><topic>Immunohistochemistry</topic><topic>Life Sciences</topic><topic>Matrix metalloproteinase</topic><topic>Metalloproteinase</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Myocardium</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-κB protein</topic><topic>Original Paper</topic><topic>Oxidative stress</topic><topic>Peroxisome proliferator-activated receptors</topic><topic>Phosphorylation</topic><topic>PPAR gamma - agonists</topic><topic>PPAR gamma - genetics</topic><topic>Rats</topic><topic>Rodents</topic><topic>Sodium</topic><topic>Transcription Factor AP-1 - 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Academic</collection><jtitle>Journal of molecular histology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Mei</au><au>Xiong, Jun</au><au>Zou, Qiang</au><au>Wang, Dan-Dan</au><au>Huang, Cong-Xin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chrysin attenuates interstitial fibrosis and improves cardiac function in a rat model of acute myocardial infarction</atitle><jtitle>Journal of molecular histology</jtitle><stitle>J Mol Hist</stitle><addtitle>J Mol Histol</addtitle><date>2018-12-01</date><risdate>2018</risdate><volume>49</volume><issue>6</issue><spage>555</spage><epage>565</epage><pages>555-565</pages><issn>1567-2379</issn><eissn>1567-2387</eissn><abstract>Interstitial fibrosis after acute myocardial infarction (MI) leads to cardiac structural remodeling and dysfunction. The peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist chrysin has been shown to protect injured myocardium through suppression of oxidative stress and inflammation. This study was designed to investigate the effect and mechanism of chrysin on myocardial fibrosis. A rat MI model was created by ligating the left coronary artery. The rats with MI were treated with chrysin (40 mg/kg/day) or 0.5% carboxymethylcellulose sodium by intragastric administration for 4 weeks after operation. The effect of chrysin on cardiac fibroblasts (CFs) were also assessed in vitro. Echocardiography showed that cardiac function was significantly improved after chrysin treatment. Chrysin reduced the levels of MDA and SOD and GSH-Px in myocardial tissue. Chrysin attenuated the interstitial and perivascular fibrosis and the expression of collagenlin the peri-infarcted zone and remarkably decreased the levels of matrix metalloproteinase-2 (MMP-2) and MMP-9. Chrysin up-regulated PPAR-γ and inhibited the nuclear factor-kappa B (NF-κB) pathway by suppressing inhibitor kappa B kinase β phosphorylation. Immunohistochemistry analysis and PCR detected downregulated expression of AP-1 after chrysin treatment. Chrysin also markedly reduced the increased α-SMA, typeland type III collagen expression of CFs mediated by AngII in vitro. In conclusion, chrysin has an antifibrosis cardioprotective effect on the infarct peripheral zone after MI. The underlined mechanism may be the up-regulation of PPAR-γ and inhibition of the NF-κB and AP1 pathway.</abstract><cop>Dordrecht</cop><pub>Springer Netherlands</pub><pmid>30225683</pmid><doi>10.1007/s10735-018-9793-0</doi><tpages>11</tpages></addata></record> |
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| subjects | Angiotensin II Animals Biomedical and Life Sciences Biomedicine Carboxymethylcellulose Cardiac function Cell Biology Collagen (type III) Coronary artery Developmental Biology Disease Models, Animal Echocardiography Enzyme inhibitors Fibroblasts Fibroblasts - drug effects Fibrosis Fibrosis - drug therapy Flavonoids - pharmacology Flavonoids - therapeutic use Gelatinase A Gelatinase B Heart - physiopathology Heart attacks Immunohistochemistry Life Sciences Matrix metalloproteinase Metalloproteinase Myocardial infarction Myocardial Infarction - drug therapy Myocardial Infarction - pathology Myocardial Infarction - physiopathology Myocardium NF-kappa B - antagonists & inhibitors NF-κB protein Original Paper Oxidative stress Peroxisome proliferator-activated receptors Phosphorylation PPAR gamma - agonists PPAR gamma - genetics Rats Rodents Sodium Transcription Factor AP-1 - antagonists & inhibitors Transcription Factor AP-1 - metabolism Transcription factors Up-Regulation - drug effects |
| title | Chrysin attenuates interstitial fibrosis and improves cardiac function in a rat model of acute myocardial infarction |
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