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Shengmai San Ameliorates Myocardial Dysfunction and Fibrosis in Diabetic db/db Mice
In this study, we mainly investigated the effects of Shengmai San (SMS) on diabetic cardiomyopathy (DCM) in db/db mice. The db/db mice were randomly divided into model group and SMS group, while C57BLKS/J inbred mice were used as controls. After 24-week treatment, blood glucose, body weight, and hea...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4856913/ https://www.ncbi.nlm.nih.gov/pubmed/27200101 http://dx.doi.org/10.1155/2016/4621235 |
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author | Zhao, Juan Cao, Tong-Tong Tian, Jing Chen, Hui-hua Zhang, Chen Wei, Hong-Chang Guo, Wei Lu, Rong |
author_facet | Zhao, Juan Cao, Tong-Tong Tian, Jing Chen, Hui-hua Zhang, Chen Wei, Hong-Chang Guo, Wei Lu, Rong |
author_sort | Zhao, Juan |
collection | PubMed |
description | In this study, we mainly investigated the effects of Shengmai San (SMS) on diabetic cardiomyopathy (DCM) in db/db mice. The db/db mice were randomly divided into model group and SMS group, while C57BLKS/J inbred mice were used as controls. After 24-week treatment, blood glucose, body weight, and heart weight were determined. Hemodynamic changes in the left ventricle were measured using catheterization. The myocardial structure and subcellular structural changes were observed by HE staining and electron microscopy; the myocardium collagen content was quantified by Masson staining. To further explore the protective mechanism of SMS, we analyzed the expression profiles of fibrotic related proteins. Compared to nondiabetic mice, db/db mice exhibited enhanced diastolic myocardial dysfunction and adverse structural remodeling. Higher expression of profibrotic proteins and lower levels of extracellular matrix degradation were also observed. After SMS oral administration for 24 weeks, cardiac dysfunction, hypertrophy, and fibrosis in diabetic mice were greatly improved. Moreover, increased profibrotic protein expression was strongly reversed by SMS treatment in db/db mice. The results demonstrate that SMS exerts a cardioprotective effect against DCM by attenuating myocardial hypertrophy and fibrosis via a TGF-β dependent pathway. |
format | Online Article Text |
id | pubmed-4856913 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-48569132016-05-19 Shengmai San Ameliorates Myocardial Dysfunction and Fibrosis in Diabetic db/db Mice Zhao, Juan Cao, Tong-Tong Tian, Jing Chen, Hui-hua Zhang, Chen Wei, Hong-Chang Guo, Wei Lu, Rong Evid Based Complement Alternat Med Research Article In this study, we mainly investigated the effects of Shengmai San (SMS) on diabetic cardiomyopathy (DCM) in db/db mice. The db/db mice were randomly divided into model group and SMS group, while C57BLKS/J inbred mice were used as controls. After 24-week treatment, blood glucose, body weight, and heart weight were determined. Hemodynamic changes in the left ventricle were measured using catheterization. The myocardial structure and subcellular structural changes were observed by HE staining and electron microscopy; the myocardium collagen content was quantified by Masson staining. To further explore the protective mechanism of SMS, we analyzed the expression profiles of fibrotic related proteins. Compared to nondiabetic mice, db/db mice exhibited enhanced diastolic myocardial dysfunction and adverse structural remodeling. Higher expression of profibrotic proteins and lower levels of extracellular matrix degradation were also observed. After SMS oral administration for 24 weeks, cardiac dysfunction, hypertrophy, and fibrosis in diabetic mice were greatly improved. Moreover, increased profibrotic protein expression was strongly reversed by SMS treatment in db/db mice. The results demonstrate that SMS exerts a cardioprotective effect against DCM by attenuating myocardial hypertrophy and fibrosis via a TGF-β dependent pathway. Hindawi Publishing Corporation 2016 2016-04-21 /pmc/articles/PMC4856913/ /pubmed/27200101 http://dx.doi.org/10.1155/2016/4621235 Text en Copyright © 2016 Juan Zhao et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Zhao, Juan Cao, Tong-Tong Tian, Jing Chen, Hui-hua Zhang, Chen Wei, Hong-Chang Guo, Wei Lu, Rong Shengmai San Ameliorates Myocardial Dysfunction and Fibrosis in Diabetic db/db Mice |
title | Shengmai San Ameliorates Myocardial Dysfunction and Fibrosis in Diabetic db/db Mice |
title_full | Shengmai San Ameliorates Myocardial Dysfunction and Fibrosis in Diabetic db/db Mice |
title_fullStr | Shengmai San Ameliorates Myocardial Dysfunction and Fibrosis in Diabetic db/db Mice |
title_full_unstemmed | Shengmai San Ameliorates Myocardial Dysfunction and Fibrosis in Diabetic db/db Mice |
title_short | Shengmai San Ameliorates Myocardial Dysfunction and Fibrosis in Diabetic db/db Mice |
title_sort | shengmai san ameliorates myocardial dysfunction and fibrosis in diabetic db/db mice |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4856913/ https://www.ncbi.nlm.nih.gov/pubmed/27200101 http://dx.doi.org/10.1155/2016/4621235 |
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