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Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway

The aim of the current study was to investigate the effect and mechanism of schisandrin B (Sch B) on myocardial hypertrophy induced by pressure overload in mice. Male C57BL/6J mice were randomly divided into three groups: i) Sham (n=12); ii) transverse aortic constriction (TAC) (n=12); and iii) Sch...

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Autores principales: Ai, Fen, Guo, Qing-Hao, Yu, Bo, Li, Wei, Guo, Xin, Chen, Zhen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6878904/
https://www.ncbi.nlm.nih.gov/pubmed/31798701
http://dx.doi.org/10.3892/etm.2019.8154
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author Ai, Fen
Guo, Qing-Hao
Yu, Bo
Li, Wei
Guo, Xin
Chen, Zhen
author_facet Ai, Fen
Guo, Qing-Hao
Yu, Bo
Li, Wei
Guo, Xin
Chen, Zhen
author_sort Ai, Fen
collection PubMed
description The aim of the current study was to investigate the effect and mechanism of schisandrin B (Sch B) on myocardial hypertrophy induced by pressure overload in mice. Male C57BL/6J mice were randomly divided into three groups: i) Sham (n=12); ii) transverse aortic constriction (TAC) (n=12); and iii) Sch B-treated (n=12; 80 mg·kg(−1)·d(−1) per gavage). The model of myocardial hypertrophy was established by constricting the descending branch of the aortic arch. Following a 4-week treatment period, cardiac remodeling was evaluated using echocardiography and pathological and molecular analysis. Sch B improved cardiac function in the Sch B-treated group compared with the TAC group. Moreover, the Sch B-treated group had a smaller myocardial cell cross-sectional area and less fibrosis compared with the TAC group. The protein expression levels of cardiac hypertrophy and fibrosis markers in the TAC group were significantly higher compared with those in the sham group. The same markers in the Sch B-treated group were significantly lower compared with those in the TAC group. Additionally, the phosphorylation levels of the mitogen-activated protein kinase (MAPK) signaling pathway-associated proteins extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase 1/2 and P38 mitogen-activated protein kinase were significantly lower in the Sch B-treated group compared with the TAC group. Further in vitro investigation demonstrated that Sch B prevented the adverse effects of angiotensin II-induced hypertrophy and fibrosis by inhibiting the MAPK signaling pathway in H9c2 cells. In conclusion, Sch B may improve pathological myocardial remodeling and cardiac function induced by pressure overload, and its underlying mechanism may be associated with inhibition of the MAPK signaling pathway.
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spelling pubmed-68789042019-12-03 Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway Ai, Fen Guo, Qing-Hao Yu, Bo Li, Wei Guo, Xin Chen, Zhen Exp Ther Med Articles The aim of the current study was to investigate the effect and mechanism of schisandrin B (Sch B) on myocardial hypertrophy induced by pressure overload in mice. Male C57BL/6J mice were randomly divided into three groups: i) Sham (n=12); ii) transverse aortic constriction (TAC) (n=12); and iii) Sch B-treated (n=12; 80 mg·kg(−1)·d(−1) per gavage). The model of myocardial hypertrophy was established by constricting the descending branch of the aortic arch. Following a 4-week treatment period, cardiac remodeling was evaluated using echocardiography and pathological and molecular analysis. Sch B improved cardiac function in the Sch B-treated group compared with the TAC group. Moreover, the Sch B-treated group had a smaller myocardial cell cross-sectional area and less fibrosis compared with the TAC group. The protein expression levels of cardiac hypertrophy and fibrosis markers in the TAC group were significantly higher compared with those in the sham group. The same markers in the Sch B-treated group were significantly lower compared with those in the TAC group. Additionally, the phosphorylation levels of the mitogen-activated protein kinase (MAPK) signaling pathway-associated proteins extracellular signal-regulated kinase 1/2, c-Jun N-terminal kinase 1/2 and P38 mitogen-activated protein kinase were significantly lower in the Sch B-treated group compared with the TAC group. Further in vitro investigation demonstrated that Sch B prevented the adverse effects of angiotensin II-induced hypertrophy and fibrosis by inhibiting the MAPK signaling pathway in H9c2 cells. In conclusion, Sch B may improve pathological myocardial remodeling and cardiac function induced by pressure overload, and its underlying mechanism may be associated with inhibition of the MAPK signaling pathway. D.A. Spandidos 2019-12 2019-10-31 /pmc/articles/PMC6878904/ /pubmed/31798701 http://dx.doi.org/10.3892/etm.2019.8154 Text en Copyright: © Ai et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Ai, Fen
Guo, Qing-Hao
Yu, Bo
Li, Wei
Guo, Xin
Chen, Zhen
Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway
title Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway
title_full Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway
title_fullStr Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway
title_full_unstemmed Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway
title_short Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway
title_sort schisandrin b attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the mapk signaling pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6878904/
https://www.ncbi.nlm.nih.gov/pubmed/31798701
http://dx.doi.org/10.3892/etm.2019.8154
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