Cargando…

Naoxintong/PPARα Signaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress

Naoxintong (NXT) is an empirical formula based on the principle of traditional Chinese medicine, which has been approved by China Food and Drug Administration (CFDA) and is widely used for treatment of patients with cerebrovascular and cardiovascular diseases in China. The aim of this study is to in...

Descripción completa

Detalles Bibliográficos
Autores principales: Xu, Huimin, Jin, Jianhua, Chen, Lu, Li, Chunxiao, Xu, Qinggang, Shi, Juanjuan, Zhao, Buchang, Hou, Yongzhong, Wang, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5030446/
https://www.ncbi.nlm.nih.gov/pubmed/27668004
http://dx.doi.org/10.1155/2016/4370381
_version_ 1782454681702760448
author Xu, Huimin
Jin, Jianhua
Chen, Lu
Li, Chunxiao
Xu, Qinggang
Shi, Juanjuan
Zhao, Buchang
Hou, Yongzhong
Wang, Hong
author_facet Xu, Huimin
Jin, Jianhua
Chen, Lu
Li, Chunxiao
Xu, Qinggang
Shi, Juanjuan
Zhao, Buchang
Hou, Yongzhong
Wang, Hong
author_sort Xu, Huimin
collection PubMed
description Naoxintong (NXT) is an empirical formula based on the principle of traditional Chinese medicine, which has been approved by China Food and Drug Administration (CFDA) and is widely used for treatment of patients with cerebrovascular and cardiovascular diseases in China. The aim of this study is to investigate the protective mechanism of NXT on H9c2 cells (cardiogenic cell line) in response to H(2)O(2). MTT, Western blot, and flow cytometry (FCM) methods were used to identify the protective effect of NXT extract on H(2)O(2)-induced H9c2 cells. Here we found that NXT extract significantly increased H9c2 cell viability and reduced H(2)O(2)-induced cell apoptosis and autophagy. More importantly, NXT inhibited H(2)O(2)-induced H9c2 cell apoptosis and autophagy by increasing PPARα protein levels. In contrast, silenced PPARα terminated NXT protective effect on H(2)O(2)-induced H9c2 cells. These findings suggest that NXT/PPARα signaling suppressed H(2)O(2)-induced H9c2 cell apoptosis and autophagy.
format Online
Article
Text
id pubmed-5030446
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher Hindawi Publishing Corporation
record_format MEDLINE/PubMed
spelling pubmed-50304462016-09-25 Naoxintong/PPARα Signaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress Xu, Huimin Jin, Jianhua Chen, Lu Li, Chunxiao Xu, Qinggang Shi, Juanjuan Zhao, Buchang Hou, Yongzhong Wang, Hong Evid Based Complement Alternat Med Research Article Naoxintong (NXT) is an empirical formula based on the principle of traditional Chinese medicine, which has been approved by China Food and Drug Administration (CFDA) and is widely used for treatment of patients with cerebrovascular and cardiovascular diseases in China. The aim of this study is to investigate the protective mechanism of NXT on H9c2 cells (cardiogenic cell line) in response to H(2)O(2). MTT, Western blot, and flow cytometry (FCM) methods were used to identify the protective effect of NXT extract on H(2)O(2)-induced H9c2 cells. Here we found that NXT extract significantly increased H9c2 cell viability and reduced H(2)O(2)-induced cell apoptosis and autophagy. More importantly, NXT inhibited H(2)O(2)-induced H9c2 cell apoptosis and autophagy by increasing PPARα protein levels. In contrast, silenced PPARα terminated NXT protective effect on H(2)O(2)-induced H9c2 cells. These findings suggest that NXT/PPARα signaling suppressed H(2)O(2)-induced H9c2 cell apoptosis and autophagy. Hindawi Publishing Corporation 2016 2016-09-07 /pmc/articles/PMC5030446/ /pubmed/27668004 http://dx.doi.org/10.1155/2016/4370381 Text en Copyright © 2016 Huimin Xu 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
Xu, Huimin
Jin, Jianhua
Chen, Lu
Li, Chunxiao
Xu, Qinggang
Shi, Juanjuan
Zhao, Buchang
Hou, Yongzhong
Wang, Hong
Naoxintong/PPARα Signaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress
title Naoxintong/PPARα Signaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress
title_full Naoxintong/PPARα Signaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress
title_fullStr Naoxintong/PPARα Signaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress
title_full_unstemmed Naoxintong/PPARα Signaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress
title_short Naoxintong/PPARα Signaling Inhibits H9c2 Cell Apoptosis and Autophagy in Response to Oxidative Stress
title_sort naoxintong/pparα signaling inhibits h9c2 cell apoptosis and autophagy in response to oxidative stress
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5030446/
https://www.ncbi.nlm.nih.gov/pubmed/27668004
http://dx.doi.org/10.1155/2016/4370381
work_keys_str_mv AT xuhuimin naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress
AT jinjianhua naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress
AT chenlu naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress
AT lichunxiao naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress
AT xuqinggang naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress
AT shijuanjuan naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress
AT zhaobuchang naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress
AT houyongzhong naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress
AT wanghong naoxintongpparasignalinginhibitsh9c2cellapoptosisandautophagyinresponsetooxidativestress