Cargando…
Yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of AMPK/mTOR-mediated autophagy
CONTEXT: Acute myocardial infarction (AMI) is defined as myocardial necrosis. Clinicians use the traditional Chinese patent medicine Yangxinkang Tablet (YXK) to treat chronic heart failure. OBJECTIVE: To explore the effects of YXK on heart injury following AMI and the underlying mechanisms. MATERIAL...
Autores principales: | , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2020
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7178820/ https://www.ncbi.nlm.nih.gov/pubmed/32285737 http://dx.doi.org/10.1080/13880209.2020.1748662 |
_version_ | 1783525544097218560 |
---|---|
author | Ren, Pei-hua Zhang, Zhi-min Wang, Peng Zhu, Han-ping Li, Zhen-qiu |
author_facet | Ren, Pei-hua Zhang, Zhi-min Wang, Peng Zhu, Han-ping Li, Zhen-qiu |
author_sort | Ren, Pei-hua |
collection | PubMed |
description | CONTEXT: Acute myocardial infarction (AMI) is defined as myocardial necrosis. Clinicians use the traditional Chinese patent medicine Yangxinkang Tablet (YXK) to treat chronic heart failure. OBJECTIVE: To explore the effects of YXK on heart injury following AMI and the underlying mechanisms. MATERIALS AND METHODS: The AMI model was produced in Wistar rats by permanent ligation of the left anterior descending coronary artery. Rats were divided into the following five groups: Sham (n = 6), MI (Model, n = 10), AICAR (AMPK agonist, 50 mg/kg/d, i.p., n = 10), Compound C (AMPK inhibitor, 10 mg/kg/d, i.p., n = 10), and YXK (0.72 g/kg/d, gavage, n = 10) groups. Cardiac function, cardiac fibrosis, apoptosis, and expression of p-AMPK, p-mTOR, and autophagy-related proteins was measured after 4 weeks of treatment after the successful modelling of the AMI. RESULTS: Compared to MI group, both YXK and AMPK inhibitor improved cardiac dysfunction and reduced cardiac fibrosis (15.6 ± 2.3; 22.6 ± 4.6 vs. 34.6 ± 4.3%) and myocardial cell apoptosis (12 ± 3.67; 25.6 ± 6.8 vs. 54 ± 4.8%). Futhermore, YXK and AMPK inhibitor significantly decreased p-AMPK expression by 11.05% and 14.64%, LC3II/I by 25.08% and 35.28% and Beclin-1 by 66.71% and 33.85%, increased p-mTOR by 22.14% and 47.46% and p62 by 70.83% and 18.58%. CONCLUSIONS: The underlying mechanism appears to include suppression of autophagy via inhibiting AMPK/mTOR signalling, suggesting that YXK may serve as a potentially effective Chinese herbal compound for suppressing cardiac fibrosis in heart injury. |
format | Online Article Text |
id | pubmed-7178820 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-71788202020-05-01 Yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of AMPK/mTOR-mediated autophagy Ren, Pei-hua Zhang, Zhi-min Wang, Peng Zhu, Han-ping Li, Zhen-qiu Pharm Biol Research Article CONTEXT: Acute myocardial infarction (AMI) is defined as myocardial necrosis. Clinicians use the traditional Chinese patent medicine Yangxinkang Tablet (YXK) to treat chronic heart failure. OBJECTIVE: To explore the effects of YXK on heart injury following AMI and the underlying mechanisms. MATERIALS AND METHODS: The AMI model was produced in Wistar rats by permanent ligation of the left anterior descending coronary artery. Rats were divided into the following five groups: Sham (n = 6), MI (Model, n = 10), AICAR (AMPK agonist, 50 mg/kg/d, i.p., n = 10), Compound C (AMPK inhibitor, 10 mg/kg/d, i.p., n = 10), and YXK (0.72 g/kg/d, gavage, n = 10) groups. Cardiac function, cardiac fibrosis, apoptosis, and expression of p-AMPK, p-mTOR, and autophagy-related proteins was measured after 4 weeks of treatment after the successful modelling of the AMI. RESULTS: Compared to MI group, both YXK and AMPK inhibitor improved cardiac dysfunction and reduced cardiac fibrosis (15.6 ± 2.3; 22.6 ± 4.6 vs. 34.6 ± 4.3%) and myocardial cell apoptosis (12 ± 3.67; 25.6 ± 6.8 vs. 54 ± 4.8%). Futhermore, YXK and AMPK inhibitor significantly decreased p-AMPK expression by 11.05% and 14.64%, LC3II/I by 25.08% and 35.28% and Beclin-1 by 66.71% and 33.85%, increased p-mTOR by 22.14% and 47.46% and p62 by 70.83% and 18.58%. CONCLUSIONS: The underlying mechanism appears to include suppression of autophagy via inhibiting AMPK/mTOR signalling, suggesting that YXK may serve as a potentially effective Chinese herbal compound for suppressing cardiac fibrosis in heart injury. Taylor & Francis 2020-04-14 /pmc/articles/PMC7178820/ /pubmed/32285737 http://dx.doi.org/10.1080/13880209.2020.1748662 Text en © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Ren, Pei-hua Zhang, Zhi-min Wang, Peng Zhu, Han-ping Li, Zhen-qiu Yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of AMPK/mTOR-mediated autophagy |
title | Yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of AMPK/mTOR-mediated autophagy |
title_full | Yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of AMPK/mTOR-mediated autophagy |
title_fullStr | Yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of AMPK/mTOR-mediated autophagy |
title_full_unstemmed | Yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of AMPK/mTOR-mediated autophagy |
title_short | Yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of AMPK/mTOR-mediated autophagy |
title_sort | yangxinkang tablet protects against cardiac dysfunction and remodelling after myocardial infarction in rats through inhibition of ampk/mtor-mediated autophagy |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7178820/ https://www.ncbi.nlm.nih.gov/pubmed/32285737 http://dx.doi.org/10.1080/13880209.2020.1748662 |
work_keys_str_mv | AT renpeihua yangxinkangtabletprotectsagainstcardiacdysfunctionandremodellingaftermyocardialinfarctioninratsthroughinhibitionofampkmtormediatedautophagy AT zhangzhimin yangxinkangtabletprotectsagainstcardiacdysfunctionandremodellingaftermyocardialinfarctioninratsthroughinhibitionofampkmtormediatedautophagy AT wangpeng yangxinkangtabletprotectsagainstcardiacdysfunctionandremodellingaftermyocardialinfarctioninratsthroughinhibitionofampkmtormediatedautophagy AT zhuhanping yangxinkangtabletprotectsagainstcardiacdysfunctionandremodellingaftermyocardialinfarctioninratsthroughinhibitionofampkmtormediatedautophagy AT lizhenqiu yangxinkangtabletprotectsagainstcardiacdysfunctionandremodellingaftermyocardialinfarctioninratsthroughinhibitionofampkmtormediatedautophagy |