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Naoxintong/PPARγ Signaling Inhibits Cardiac Hypertrophy via Activation of Autophagy

As a traditional Chinese medicine, Naoxintong capsule (NXT) has been approved by China Food and Drug Administration (CFDA), which is used for cardiocerebrovascular disease treatment. Here we found that NXT extract significantly promoted H9c2 cardiomyocyte cell autophagy involved in increased autopha...

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Detalles Bibliográficos
Autores principales: Yuan, Shuping, Jin, Jianhua, Chen, Lu, Hou, Yongzhong, Wang, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5331281/
https://www.ncbi.nlm.nih.gov/pubmed/28293264
http://dx.doi.org/10.1155/2017/3801976
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author Yuan, Shuping
Jin, Jianhua
Chen, Lu
Hou, Yongzhong
Wang, Hong
author_facet Yuan, Shuping
Jin, Jianhua
Chen, Lu
Hou, Yongzhong
Wang, Hong
author_sort Yuan, Shuping
collection PubMed
description As a traditional Chinese medicine, Naoxintong capsule (NXT) has been approved by China Food and Drug Administration (CFDA), which is used for cardiocerebrovascular disease treatment. Here we found that NXT extract significantly promoted H9c2 cardiomyocyte cell autophagy involved in increased autophagy-associated gene expression leading to inhibition of mTOR signaling. Moreover, NXT extract increased PPARγ protein expression and transcription activity of H9c2 cell. Consistent with this, in PPARγ gene silenced H9c2 cells, NXT had no effect on autophagy and mTOR signaling. Furthermore, NXT/PPARγ-mediated H9c2 autophagy led to inhibition of cardiomyocyte cell hypertrophy. These findings suggest that the extract of NXT inhibited H9c2 cardiomyocyte cell hypertrophy via PPARγ-mediated cell autophagy.
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spelling pubmed-53312812017-03-14 Naoxintong/PPARγ Signaling Inhibits Cardiac Hypertrophy via Activation of Autophagy Yuan, Shuping Jin, Jianhua Chen, Lu Hou, Yongzhong Wang, Hong Evid Based Complement Alternat Med Research Article As a traditional Chinese medicine, Naoxintong capsule (NXT) has been approved by China Food and Drug Administration (CFDA), which is used for cardiocerebrovascular disease treatment. Here we found that NXT extract significantly promoted H9c2 cardiomyocyte cell autophagy involved in increased autophagy-associated gene expression leading to inhibition of mTOR signaling. Moreover, NXT extract increased PPARγ protein expression and transcription activity of H9c2 cell. Consistent with this, in PPARγ gene silenced H9c2 cells, NXT had no effect on autophagy and mTOR signaling. Furthermore, NXT/PPARγ-mediated H9c2 autophagy led to inhibition of cardiomyocyte cell hypertrophy. These findings suggest that the extract of NXT inhibited H9c2 cardiomyocyte cell hypertrophy via PPARγ-mediated cell autophagy. Hindawi Publishing Corporation 2017 2017-02-15 /pmc/articles/PMC5331281/ /pubmed/28293264 http://dx.doi.org/10.1155/2017/3801976 Text en Copyright © 2017 Shuping Yuan 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
Yuan, Shuping
Jin, Jianhua
Chen, Lu
Hou, Yongzhong
Wang, Hong
Naoxintong/PPARγ Signaling Inhibits Cardiac Hypertrophy via Activation of Autophagy
title Naoxintong/PPARγ Signaling Inhibits Cardiac Hypertrophy via Activation of Autophagy
title_full Naoxintong/PPARγ Signaling Inhibits Cardiac Hypertrophy via Activation of Autophagy
title_fullStr Naoxintong/PPARγ Signaling Inhibits Cardiac Hypertrophy via Activation of Autophagy
title_full_unstemmed Naoxintong/PPARγ Signaling Inhibits Cardiac Hypertrophy via Activation of Autophagy
title_short Naoxintong/PPARγ Signaling Inhibits Cardiac Hypertrophy via Activation of Autophagy
title_sort naoxintong/pparγ signaling inhibits cardiac hypertrophy via activation of autophagy
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5331281/
https://www.ncbi.nlm.nih.gov/pubmed/28293264
http://dx.doi.org/10.1155/2017/3801976
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