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Active components from Radix Scrophulariae inhibits the ventricular remodeling induced by hypertension in rats
BACKGROUND: In the previous study, active extract of Radix Scrophularia (ACRS) demonstrated beneficial effects on ventricular remodeling induced by coronary artery ligation and lowered blood pressure in rats. And ACRS also exhibited the effect on lowering the blood pressure in spontaneously hyperten...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801831/ https://www.ncbi.nlm.nih.gov/pubmed/27066371 http://dx.doi.org/10.1186/s40064-016-1985-z |
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author | Zhang, Chao Chao Gu, Wei Liang Wu, Xi Min Li, Yi Ming Chen, Chang Xun Huang, Xiao Yan |
author_facet | Zhang, Chao Chao Gu, Wei Liang Wu, Xi Min Li, Yi Ming Chen, Chang Xun Huang, Xiao Yan |
author_sort | Zhang, Chao Chao |
collection | PubMed |
description | BACKGROUND: In the previous study, active extract of Radix Scrophularia (ACRS) demonstrated beneficial effects on ventricular remodeling induced by coronary artery ligation and lowered blood pressure in rats. And ACRS also exhibited the effect on lowering the blood pressure in spontaneously hypertensive rats (SHRs). The aim of this study is to explore the effects of ACRS on ventricular remodeling in SHRs and underlying mechanisms. RESULTS: ACRS significantly lowered the blood pressure, decreased the heart mass indexes, inhibited the deposition of perivascular and interstitial, attenuated the accumulation of types I and III collagen, reduced the tissue angiotensin II, serum norepinephrine and tumor necrosis factor-α concentrations. The underlying mechanisms may be related to downregulating the mRNA expressions of collagen type I, transforming growth factor-β1 and angiotensin converting enzyme, suppressing the phosphorylation of extracellular signal regulated kinase 1/2, c-Jun N-terminal kinase (JNK/SAPK) and p38 mitogen-activated protein kinases (p38 MAPK). CONCLUSION: Continuous treatment of SHRs with ACRS for 21 weeks reduced blood pressure, myocardial hypertrophy and the amount of interstitial and perivascular collagen, which indicated that ACRS could prevent hypertensive ventricular remodeling. This can be attributed to suppression of the sympathetic nervous and renin angiotensin aldosterone system through the inhibition of ERK 1/2, JNK and p38 MAPK pathways. |
format | Online Article Text |
id | pubmed-4801831 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-48018312016-04-09 Active components from Radix Scrophulariae inhibits the ventricular remodeling induced by hypertension in rats Zhang, Chao Chao Gu, Wei Liang Wu, Xi Min Li, Yi Ming Chen, Chang Xun Huang, Xiao Yan Springerplus Research BACKGROUND: In the previous study, active extract of Radix Scrophularia (ACRS) demonstrated beneficial effects on ventricular remodeling induced by coronary artery ligation and lowered blood pressure in rats. And ACRS also exhibited the effect on lowering the blood pressure in spontaneously hypertensive rats (SHRs). The aim of this study is to explore the effects of ACRS on ventricular remodeling in SHRs and underlying mechanisms. RESULTS: ACRS significantly lowered the blood pressure, decreased the heart mass indexes, inhibited the deposition of perivascular and interstitial, attenuated the accumulation of types I and III collagen, reduced the tissue angiotensin II, serum norepinephrine and tumor necrosis factor-α concentrations. The underlying mechanisms may be related to downregulating the mRNA expressions of collagen type I, transforming growth factor-β1 and angiotensin converting enzyme, suppressing the phosphorylation of extracellular signal regulated kinase 1/2, c-Jun N-terminal kinase (JNK/SAPK) and p38 mitogen-activated protein kinases (p38 MAPK). CONCLUSION: Continuous treatment of SHRs with ACRS for 21 weeks reduced blood pressure, myocardial hypertrophy and the amount of interstitial and perivascular collagen, which indicated that ACRS could prevent hypertensive ventricular remodeling. This can be attributed to suppression of the sympathetic nervous and renin angiotensin aldosterone system through the inhibition of ERK 1/2, JNK and p38 MAPK pathways. Springer International Publishing 2016-03-22 /pmc/articles/PMC4801831/ /pubmed/27066371 http://dx.doi.org/10.1186/s40064-016-1985-z Text en © Zhang et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Research Zhang, Chao Chao Gu, Wei Liang Wu, Xi Min Li, Yi Ming Chen, Chang Xun Huang, Xiao Yan Active components from Radix Scrophulariae inhibits the ventricular remodeling induced by hypertension in rats |
title | Active components from Radix Scrophulariae inhibits the ventricular remodeling induced by hypertension in rats |
title_full | Active components from Radix Scrophulariae inhibits the ventricular remodeling induced by hypertension in rats |
title_fullStr | Active components from Radix Scrophulariae inhibits the ventricular remodeling induced by hypertension in rats |
title_full_unstemmed | Active components from Radix Scrophulariae inhibits the ventricular remodeling induced by hypertension in rats |
title_short | Active components from Radix Scrophulariae inhibits the ventricular remodeling induced by hypertension in rats |
title_sort | active components from radix scrophulariae inhibits the ventricular remodeling induced by hypertension in rats |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4801831/ https://www.ncbi.nlm.nih.gov/pubmed/27066371 http://dx.doi.org/10.1186/s40064-016-1985-z |
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