Sacubitril/valsartan reverses cardiac structure and function in experimental model of hypertension-induced hypertrophic cardiomyopathy
This study evaluated the effect of sacubtril/valsartan on cardiac remodeling, molecular and cellular adaptations in experimental (rat) model of hypertension-induced hypertrophic cardiomyopathy. Thirty Wistar Kyoto rats, 10 healthy (control) and 20 rats with confirmed hypertension-induced hypertrop...
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creator | Jeremic, Jovana Govoruskina, Natalia Bradic, Jovana Milosavljevic, Isidora Srejovic, Ivan Zivkovic, Vladimir Jeremic, Nevena Nikolic Turnic, Tamara Tanaskovic, Irena Bolevich, Stefani Jakovljevic, Vladimir Bolevich, Sergey Zivanovic, Marko N. Okwose, Nduka Seklic, Dragana Milivojevic, Nevena Grujic, Jelena Velicki, Lazar MacGowan, Guy Jakovljevic, Djordje G. Filipovic, Nenad |
description | This study evaluated the effect of sacubtril/valsartan on cardiac remodeling, molecular and cellular adaptations in experimental (rat) model of hypertension-induced hypertrophic cardiomyopathy. Thirty
Wistar Kyoto
rats, 10 healthy (control) and 20 rats with confirmed hypertension-induced hypertrophic cardiomyopathy (HpCM), were used for this study. The HpCM group was further subdivided into untreated and sacubitril/valsartan-treated groups. Myocardial structure and function were assessed using echocardiography, Langendorff’s isolated heart experiment, blood sampling and qualitative polymerase chain reaction. Echocardiographic examinations revealed protective effects of sacubitril/valsartan by improving left ventricular internal diameter in systole and diastole and fractional shortening. Additionally, sacubitril/valsartan treatment decreased systolic and diastolic blood pressures in comparison with untreated hypertensive rats. Moreover, sacubitril/valsartan treatment reduced oxidative stress and apoptosis (reduced expression of Bax and Cas9 genes) compared to untreated rats. There was a regular histomorphology of cardiomyocytes, interstitium, and blood vessels in treated rats compared to untreated HpCM rats which expressed hypertrophic cardiomyocytes, with polymorphic nuclei, prominent nucleoli and moderately dilated interstitium. In experimental model of hypertension-induced hypertrophic cardiomyopathy, sacubitril/valsartan treatment led to improved cardiac structure, haemodynamic performance, and reduced oxidative stress and apoptosis. Sacubitril/valsartan thus presents as a potential therapeutic strategy resulted in hypertension-induced hypertrophic cardiomyopathy. |
doi_str_mv | 10.1007/s11010-023-04690-7 |
format | Article |
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Wistar Kyoto
rats, 10 healthy (control) and 20 rats with confirmed hypertension-induced hypertrophic cardiomyopathy (HpCM), were used for this study. The HpCM group was further subdivided into untreated and sacubitril/valsartan-treated groups. Myocardial structure and function were assessed using echocardiography, Langendorff’s isolated heart experiment, blood sampling and qualitative polymerase chain reaction. Echocardiographic examinations revealed protective effects of sacubitril/valsartan by improving left ventricular internal diameter in systole and diastole and fractional shortening. Additionally, sacubitril/valsartan treatment decreased systolic and diastolic blood pressures in comparison with untreated hypertensive rats. Moreover, sacubitril/valsartan treatment reduced oxidative stress and apoptosis (reduced expression of Bax and Cas9 genes) compared to untreated rats. There was a regular histomorphology of cardiomyocytes, interstitium, and blood vessels in treated rats compared to untreated HpCM rats which expressed hypertrophic cardiomyocytes, with polymorphic nuclei, prominent nucleoli and moderately dilated interstitium. In experimental model of hypertension-induced hypertrophic cardiomyopathy, sacubitril/valsartan treatment led to improved cardiac structure, haemodynamic performance, and reduced oxidative stress and apoptosis. Sacubitril/valsartan thus presents as a potential therapeutic strategy resulted in hypertension-induced hypertrophic cardiomyopathy.</description><identifier>ISSN: 0300-8177</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-023-04690-7</identifier><identifier>PMID: 36997815</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Analysis ; Animal models ; Apoptosis ; BAX protein ; Biochemistry ; Biomedical and Life Sciences ; Blood ; Blood vessels ; Cancer Research ; Cardiology ; Cardiomyocytes ; Cardiomyopathy ; Cardiomyopathy, Hypertrophic ; Complications and side effects ; Diastole ; Echocardiography ; Genes ; Heart ; Hemodynamics ; Hypertension ; Life Sciences ; Medical Biochemistry ; Medical examination ; Nucleoli ; Oxidative stress ; Polymerase chain reaction ; Structure-function relationships ; Systole ; Valsartan ; Ventricle</subject><ispartof>Molecular and cellular biochemistry, 2023-12, Vol.478 (12), p.2645-2656</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. 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Thirty
Wistar Kyoto
rats, 10 healthy (control) and 20 rats with confirmed hypertension-induced hypertrophic cardiomyopathy (HpCM), were used for this study. The HpCM group was further subdivided into untreated and sacubitril/valsartan-treated groups. Myocardial structure and function were assessed using echocardiography, Langendorff’s isolated heart experiment, blood sampling and qualitative polymerase chain reaction. Echocardiographic examinations revealed protective effects of sacubitril/valsartan by improving left ventricular internal diameter in systole and diastole and fractional shortening. Additionally, sacubitril/valsartan treatment decreased systolic and diastolic blood pressures in comparison with untreated hypertensive rats. Moreover, sacubitril/valsartan treatment reduced oxidative stress and apoptosis (reduced expression of Bax and Cas9 genes) compared to untreated rats. There was a regular histomorphology of cardiomyocytes, interstitium, and blood vessels in treated rats compared to untreated HpCM rats which expressed hypertrophic cardiomyocytes, with polymorphic nuclei, prominent nucleoli and moderately dilated interstitium. In experimental model of hypertension-induced hypertrophic cardiomyopathy, sacubitril/valsartan treatment led to improved cardiac structure, haemodynamic performance, and reduced oxidative stress and apoptosis. Sacubitril/valsartan thus presents as a potential therapeutic strategy resulted in hypertension-induced hypertrophic cardiomyopathy.</description><subject>Analysis</subject><subject>Animal models</subject><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Blood</subject><subject>Blood vessels</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiomyopathy, Hypertrophic</subject><subject>Complications and side effects</subject><subject>Diastole</subject><subject>Echocardiography</subject><subject>Genes</subject><subject>Heart</subject><subject>Hemodynamics</subject><subject>Hypertension</subject><subject>Life Sciences</subject><subject>Medical Biochemistry</subject><subject>Medical examination</subject><subject>Nucleoli</subject><subject>Oxidative stress</subject><subject>Polymerase chain 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reverses cardiac structure and function in experimental model of hypertension-induced hypertrophic cardiomyopathy</title><author>Jeremic, Jovana ; Govoruskina, Natalia ; Bradic, Jovana ; Milosavljevic, Isidora ; Srejovic, Ivan ; Zivkovic, Vladimir ; Jeremic, Nevena ; Nikolic Turnic, Tamara ; Tanaskovic, Irena ; Bolevich, Stefani ; Jakovljevic, Vladimir ; Bolevich, Sergey ; Zivanovic, Marko N. ; Okwose, Nduka ; Seklic, Dragana ; Milivojevic, Nevena ; Grujic, Jelena ; Velicki, Lazar ; MacGowan, Guy ; Jakovljevic, Djordje G. ; Filipovic, Nenad</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-55dc1ece23396411b5e11dcdc1a86e974eaeb1d3f5b55f92b5264bbaf616605e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Analysis</topic><topic>Animal models</topic><topic>Apoptosis</topic><topic>BAX protein</topic><topic>Biochemistry</topic><topic>Biomedical and Life 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Biochem</addtitle><date>2023-12-01</date><risdate>2023</risdate><volume>478</volume><issue>12</issue><spage>2645</spage><epage>2656</epage><pages>2645-2656</pages><issn>0300-8177</issn><eissn>1573-4919</eissn><abstract>This study evaluated the effect of sacubtril/valsartan on cardiac remodeling, molecular and cellular adaptations in experimental (rat) model of hypertension-induced hypertrophic cardiomyopathy. Thirty
Wistar Kyoto
rats, 10 healthy (control) and 20 rats with confirmed hypertension-induced hypertrophic cardiomyopathy (HpCM), were used for this study. The HpCM group was further subdivided into untreated and sacubitril/valsartan-treated groups. Myocardial structure and function were assessed using echocardiography, Langendorff’s isolated heart experiment, blood sampling and qualitative polymerase chain reaction. Echocardiographic examinations revealed protective effects of sacubitril/valsartan by improving left ventricular internal diameter in systole and diastole and fractional shortening. Additionally, sacubitril/valsartan treatment decreased systolic and diastolic blood pressures in comparison with untreated hypertensive rats. Moreover, sacubitril/valsartan treatment reduced oxidative stress and apoptosis (reduced expression of Bax and Cas9 genes) compared to untreated rats. There was a regular histomorphology of cardiomyocytes, interstitium, and blood vessels in treated rats compared to untreated HpCM rats which expressed hypertrophic cardiomyocytes, with polymorphic nuclei, prominent nucleoli and moderately dilated interstitium. In experimental model of hypertension-induced hypertrophic cardiomyopathy, sacubitril/valsartan treatment led to improved cardiac structure, haemodynamic performance, and reduced oxidative stress and apoptosis. Sacubitril/valsartan thus presents as a potential therapeutic strategy resulted in hypertension-induced hypertrophic cardiomyopathy.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36997815</pmid><doi>10.1007/s11010-023-04690-7</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Analysis Animal models Apoptosis BAX protein Biochemistry Biomedical and Life Sciences Blood Blood vessels Cancer Research Cardiology Cardiomyocytes Cardiomyopathy Cardiomyopathy, Hypertrophic Complications and side effects Diastole Echocardiography Genes Heart Hemodynamics Hypertension Life Sciences Medical Biochemistry Medical examination Nucleoli Oxidative stress Polymerase chain reaction Structure-function relationships Systole Valsartan Ventricle |
title | Sacubitril/valsartan reverses cardiac structure and function in experimental model of hypertension-induced hypertrophic cardiomyopathy |
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