The effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone on the pressure overload-induced progression of cardiac hypertrophy to cardiac failure
We investigated the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC), which was isolated from the roots of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z.Wei (Papilionaceae) (MKL), on the progression of cardiac hypertrophy to failure in a rat model of abdominal aortic banding (AA...
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| creator | Huang, Jianchun Tang, XiaoJun Liang, Xingmei Wen, Qingwei Zhang, Shijun Xuan, Feifei Jian, Jie Lin, Xing Huang, Renbin |
| description | We investigated the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC), which was isolated from the roots of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z.Wei (Papilionaceae) (MKL), on the progression of cardiac hypertrophy to failure in a rat model of abdominal aortic banding (AAB)-induced pressure overloading. Endothelial dysfunction is central to pressure overload-induced cardiac hypertrophy and failure. It would be useful to clarify whether MHBFC could prevent this dysfunction. The effects of pressure overload were assessed in male Sprague-Dawley rats 6 weeks after AAB using the progression of cardiac hypertrophy to heart failure as the endpoint. The AAB-treated rats exhibited a greater progression to heart failure and had significantly elevated blood pressure, systolic and diastolic cardiac dysfunction, and evidence of left ventricular hypertrophy (LVH). LVH was characterized by increases in the ratios of heart and left ventricular weights to body weight, increased myocyte cross-sectional areas, myocardial and perivascular fibrosis, and elevated cardiac hydroxyproline. These symptoms could be prevented by treatment with MHBFC at daily oral doses of 6 and 12 mg/kg for 6 weeks. The progression to cardiac failure, which was demonstrated by increases in relative lung and right ventricular weights, cardiac function disorders and overexpression of atrial natriuretic peptide (ANP) mRNA, could also be prevented. Furthermore, MHBFC partialy rescued the downregulated nitric oxide signaling system, whereas inhibited the upregulated endothelin signaling system, normalizing the balance between these two systems. MHBFC protected the endothelium and prevented the pressure overload-induced progression of cardiac hypertrophy to cardiac failure. |
| doi_str_mv | 10.1371/journal.pone.0091834 |
| format | Article |
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Kurz var. Laxior (Dunn) Z.Wei (Papilionaceae) (MKL), on the progression of cardiac hypertrophy to failure in a rat model of abdominal aortic banding (AAB)-induced pressure overloading. Endothelial dysfunction is central to pressure overload-induced cardiac hypertrophy and failure. It would be useful to clarify whether MHBFC could prevent this dysfunction. The effects of pressure overload were assessed in male Sprague-Dawley rats 6 weeks after AAB using the progression of cardiac hypertrophy to heart failure as the endpoint. The AAB-treated rats exhibited a greater progression to heart failure and had significantly elevated blood pressure, systolic and diastolic cardiac dysfunction, and evidence of left ventricular hypertrophy (LVH). LVH was characterized by increases in the ratios of heart and left ventricular weights to body weight, increased myocyte cross-sectional areas, myocardial and perivascular fibrosis, and elevated cardiac hydroxyproline. These symptoms could be prevented by treatment with MHBFC at daily oral doses of 6 and 12 mg/kg for 6 weeks. The progression to cardiac failure, which was demonstrated by increases in relative lung and right ventricular weights, cardiac function disorders and overexpression of atrial natriuretic peptide (ANP) mRNA, could also be prevented. Furthermore, MHBFC partialy rescued the downregulated nitric oxide signaling system, whereas inhibited the upregulated endothelin signaling system, normalizing the balance between these two systems. MHBFC protected the endothelium and prevented the pressure overload-induced progression of cardiac hypertrophy to cardiac failure.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0091834</identifier><identifier>PMID: 24622486</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Aorta ; Aorta - drug effects ; Aorta - pathology ; Aorta - physiopathology ; Atrial natriuretic peptide ; Banding ; Benzene ; Biology ; Blood pressure ; Blood Pressure - drug effects ; Body weight ; Cardiomegaly - complications ; Cardiomegaly - metabolism ; Cardiomegaly - pathology ; Cardiomegaly - physiopathology ; Cardiovascular disease ; Chalcones - pharmacology ; Disease Progression ; Endothelin ; Endothelins ; Endothelium ; Endothelium - drug effects ; Endothelium - metabolism ; Fibrosis ; Heart ; Heart diseases ; Heart failure ; Heart Failure - complications ; Heart Failure - prevention & control ; Heart hypertrophy ; Heart Ventricles - drug effects ; Heart Ventricles - pathology ; Hemodynamics - drug effects ; Hydroxyproline ; Hypertension ; Hypertrophy ; Lungs ; Male ; Medicine ; mRNA ; Nitric oxide ; Nitric Oxide - metabolism ; Normalizing ; Overloading ; Pharmaceuticals ; Pressure effects ; Rats ; Rats, Sprague-Dawley ; Rodents ; Signaling ; Vascular Remodeling - drug effects ; Ventricle</subject><ispartof>PloS one, 2014-03, Vol.9 (3), p.e91834-e91834</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Huang et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Huang et al 2014 Huang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-d775cd1bee28b7ddf7bc1f4ae674e8188eb712f50d103fb5ecbafe6aa5a5039a3</citedby><cites>FETCH-LOGICAL-c692t-d775cd1bee28b7ddf7bc1f4ae674e8188eb712f50d103fb5ecbafe6aa5a5039a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3951494/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3951494/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24622486$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Quintas, Luis Eduardo M.</contributor><creatorcontrib>Huang, Jianchun</creatorcontrib><creatorcontrib>Tang, XiaoJun</creatorcontrib><creatorcontrib>Liang, Xingmei</creatorcontrib><creatorcontrib>Wen, Qingwei</creatorcontrib><creatorcontrib>Zhang, Shijun</creatorcontrib><creatorcontrib>Xuan, Feifei</creatorcontrib><creatorcontrib>Jian, Jie</creatorcontrib><creatorcontrib>Lin, Xing</creatorcontrib><creatorcontrib>Huang, Renbin</creatorcontrib><title>The effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone on the pressure overload-induced progression of cardiac hypertrophy to cardiac failure</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>We investigated the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC), which was isolated from the roots of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z.Wei (Papilionaceae) (MKL), on the progression of cardiac hypertrophy to failure in a rat model of abdominal aortic banding (AAB)-induced pressure overloading. Endothelial dysfunction is central to pressure overload-induced cardiac hypertrophy and failure. It would be useful to clarify whether MHBFC could prevent this dysfunction. The effects of pressure overload were assessed in male Sprague-Dawley rats 6 weeks after AAB using the progression of cardiac hypertrophy to heart failure as the endpoint. The AAB-treated rats exhibited a greater progression to heart failure and had significantly elevated blood pressure, systolic and diastolic cardiac dysfunction, and evidence of left ventricular hypertrophy (LVH). LVH was characterized by increases in the ratios of heart and left ventricular weights to body weight, increased myocyte cross-sectional areas, myocardial and perivascular fibrosis, and elevated cardiac hydroxyproline. These symptoms could be prevented by treatment with MHBFC at daily oral doses of 6 and 12 mg/kg for 6 weeks. The progression to cardiac failure, which was demonstrated by increases in relative lung and right ventricular weights, cardiac function disorders and overexpression of atrial natriuretic peptide (ANP) mRNA, could also be prevented. Furthermore, MHBFC partialy rescued the downregulated nitric oxide signaling system, whereas inhibited the upregulated endothelin signaling system, normalizing the balance between these two systems. MHBFC protected the endothelium and prevented the pressure overload-induced progression of cardiac hypertrophy to cardiac failure.</description><subject>Analysis</subject><subject>Animals</subject><subject>Aorta</subject><subject>Aorta - drug effects</subject><subject>Aorta - pathology</subject><subject>Aorta - physiopathology</subject><subject>Atrial natriuretic peptide</subject><subject>Banding</subject><subject>Benzene</subject><subject>Biology</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Body weight</subject><subject>Cardiomegaly - complications</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomegaly - pathology</subject><subject>Cardiomegaly - physiopathology</subject><subject>Cardiovascular disease</subject><subject>Chalcones - pharmacology</subject><subject>Disease Progression</subject><subject>Endothelin</subject><subject>Endothelins</subject><subject>Endothelium</subject><subject>Endothelium - drug effects</subject><subject>Endothelium - metabolism</subject><subject>Fibrosis</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart Failure - complications</subject><subject>Heart Failure - prevention & control</subject><subject>Heart hypertrophy</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - pathology</subject><subject>Hemodynamics - drug effects</subject><subject>Hydroxyproline</subject><subject>Hypertension</subject><subject>Hypertrophy</subject><subject>Lungs</subject><subject>Male</subject><subject>Medicine</subject><subject>mRNA</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Normalizing</subject><subject>Overloading</subject><subject>Pharmaceuticals</subject><subject>Pressure effects</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Signaling</subject><subject>Vascular Remodeling - drug effects</subject><subject>Ventricle</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</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><sourceid>DOA</sourceid><recordid>eNqNk9-L1DAQx4so3rn6H4gWBNGHrknTNu2LcBz-WDg40NPXkCaTbY5ssybpcet_4X9settbtnIPkocmM5_5TjOZSZKXGC0xofjDtR1cz81ya3tYItTgmhSPklPckDyrckQeH-1PkmfeXyNUkrqqniYneVHleVFXp8mfqw5SUApE8KlVKabZBkJnb3cmo1m3ky5usxb639BDpgbHe9FxI2LS1PZpiNFbB94PLp5vwBnLZaZ7OQiQ0WPXo1NHMmoL7qTmIu12W3DB2W23S4M9mBXXJso8T54objy8mL6L5MfnT1fnX7OLyy-r87OLTFRNHjJJaSkkbgHyuqVSKtoKrAoOFS2gxnUNLcW5KpHEiKi2BNFyBRXnJS8RaThZJK_3ultjPZuq6RkuUVXjpiBVJFZ7Qlp-zbZOb7jbMcs1uzNYt2bcBS0MsHrMD01LJIUix1VbU1FKaFAuFFKoiFofp2xDuwEpoA-Om5no3NPrjq3tDSNNiYtmFHg3CTj7awAf2EZ7AcbwHuxw99-UNmWDcETf_IM-fLuJWvN4Ad0rG_OKUZSdFbSmFJHYL4tk-QAVl4SNHrtA6WifBbyfBUQmwG1Y88F7tvr-7f_Zy59z9u0R2wE3ofPWDCE2l5-DxR4UznrvQB2KjBEbJ-e-GmycHDZNTgx7dfxAh6D7USF_ASkfF9A</recordid><startdate>20140312</startdate><enddate>20140312</enddate><creator>Huang, Jianchun</creator><creator>Tang, XiaoJun</creator><creator>Liang, Xingmei</creator><creator>Wen, Qingwei</creator><creator>Zhang, Shijun</creator><creator>Xuan, Feifei</creator><creator>Jian, Jie</creator><creator>Lin, Xing</creator><creator>Huang, Renbin</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20140312</creationdate><title>The effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone on the pressure overload-induced progression of cardiac hypertrophy to cardiac failure</title><author>Huang, Jianchun ; Tang, XiaoJun ; Liang, Xingmei ; Wen, Qingwei ; Zhang, Shijun ; Xuan, Feifei ; Jian, Jie ; Lin, Xing ; Huang, Renbin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-d775cd1bee28b7ddf7bc1f4ae674e8188eb712f50d103fb5ecbafe6aa5a5039a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Aorta</topic><topic>Aorta - drug effects</topic><topic>Aorta - pathology</topic><topic>Aorta - physiopathology</topic><topic>Atrial natriuretic peptide</topic><topic>Banding</topic><topic>Benzene</topic><topic>Biology</topic><topic>Blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>Body weight</topic><topic>Cardiomegaly - complications</topic><topic>Cardiomegaly - metabolism</topic><topic>Cardiomegaly - pathology</topic><topic>Cardiomegaly - physiopathology</topic><topic>Cardiovascular disease</topic><topic>Chalcones - pharmacology</topic><topic>Disease Progression</topic><topic>Endothelin</topic><topic>Endothelins</topic><topic>Endothelium</topic><topic>Endothelium - drug effects</topic><topic>Endothelium - metabolism</topic><topic>Fibrosis</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Heart Failure - complications</topic><topic>Heart Failure - prevention & control</topic><topic>Heart hypertrophy</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Jianchun</au><au>Tang, XiaoJun</au><au>Liang, Xingmei</au><au>Wen, Qingwei</au><au>Zhang, Shijun</au><au>Xuan, Feifei</au><au>Jian, Jie</au><au>Lin, Xing</au><au>Huang, Renbin</au><au>Quintas, Luis Eduardo M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone on the pressure overload-induced progression of cardiac hypertrophy to cardiac failure</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2014-03-12</date><risdate>2014</risdate><volume>9</volume><issue>3</issue><spage>e91834</spage><epage>e91834</epage><pages>e91834-e91834</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>We investigated the effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone (MHBFC), which was isolated from the roots of Millettia pulchra (Benth.) Kurz var. Laxior (Dunn) Z.Wei (Papilionaceae) (MKL), on the progression of cardiac hypertrophy to failure in a rat model of abdominal aortic banding (AAB)-induced pressure overloading. Endothelial dysfunction is central to pressure overload-induced cardiac hypertrophy and failure. It would be useful to clarify whether MHBFC could prevent this dysfunction. The effects of pressure overload were assessed in male Sprague-Dawley rats 6 weeks after AAB using the progression of cardiac hypertrophy to heart failure as the endpoint. The AAB-treated rats exhibited a greater progression to heart failure and had significantly elevated blood pressure, systolic and diastolic cardiac dysfunction, and evidence of left ventricular hypertrophy (LVH). LVH was characterized by increases in the ratios of heart and left ventricular weights to body weight, increased myocyte cross-sectional areas, myocardial and perivascular fibrosis, and elevated cardiac hydroxyproline. These symptoms could be prevented by treatment with MHBFC at daily oral doses of 6 and 12 mg/kg for 6 weeks. The progression to cardiac failure, which was demonstrated by increases in relative lung and right ventricular weights, cardiac function disorders and overexpression of atrial natriuretic peptide (ANP) mRNA, could also be prevented. Furthermore, MHBFC partialy rescued the downregulated nitric oxide signaling system, whereas inhibited the upregulated endothelin signaling system, normalizing the balance between these two systems. MHBFC protected the endothelium and prevented the pressure overload-induced progression of cardiac hypertrophy to cardiac failure.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24622486</pmid><doi>10.1371/journal.pone.0091834</doi><tpages>e91834</tpages><oa>free_for_read</oa></addata></record> |
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| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1506819436 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Analysis Animals Aorta Aorta - drug effects Aorta - pathology Aorta - physiopathology Atrial natriuretic peptide Banding Benzene Biology Blood pressure Blood Pressure - drug effects Body weight Cardiomegaly - complications Cardiomegaly - metabolism Cardiomegaly - pathology Cardiomegaly - physiopathology Cardiovascular disease Chalcones - pharmacology Disease Progression Endothelin Endothelins Endothelium Endothelium - drug effects Endothelium - metabolism Fibrosis Heart Heart diseases Heart failure Heart Failure - complications Heart Failure - prevention & control Heart hypertrophy Heart Ventricles - drug effects Heart Ventricles - pathology Hemodynamics - drug effects Hydroxyproline Hypertension Hypertrophy Lungs Male Medicine mRNA Nitric oxide Nitric Oxide - metabolism Normalizing Overloading Pharmaceuticals Pressure effects Rats Rats, Sprague-Dawley Rodents Signaling Vascular Remodeling - drug effects Ventricle |
| title | The effects of 17-methoxyl-7-hydroxy-benzene-furanchalcone on the pressure overload-induced progression of cardiac hypertrophy to cardiac failure |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-18T16%3A03%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20effects%20of%2017-methoxyl-7-hydroxy-benzene-furanchalcone%20on%20the%20pressure%20overload-induced%20progression%20of%20cardiac%20hypertrophy%20to%20cardiac%20failure&rft.jtitle=PloS%20one&rft.au=Huang,%20Jianchun&rft.date=2014-03-12&rft.volume=9&rft.issue=3&rft.spage=e91834&rft.epage=e91834&rft.pages=e91834-e91834&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0091834&rft_dat=%3Cgale_plos_%3EA478770305%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1506819436&rft_id=info:pmid/24622486&rft_galeid=A478770305&rft_doaj_id=oai_doaj_org_article_8df7be9b3d7e4216b87c5de902cf0f04&rfr_iscdi=true |