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Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy
Ischemic heart disease is a leading cause of mortality and morbidity worldwide. We previously demonstrated that acacetin protects against myocardial ischemia reperfusion injury in rats, although the underlying mechanism remains to be elucidated. In the present study, we investigated the effects of a...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8263275/ https://www.ncbi.nlm.nih.gov/pubmed/34307696 http://dx.doi.org/10.1155/2021/9979843 |
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author | Liu, Chong Zhang, Minmin Ye, Shenyi Hong, Chenliang Chen, Jiaxi Lu, Ruyue Hu, Bingjie Yang, Weijun Shen, Bo Gu, Zhengyi |
author_facet | Liu, Chong Zhang, Minmin Ye, Shenyi Hong, Chenliang Chen, Jiaxi Lu, Ruyue Hu, Bingjie Yang, Weijun Shen, Bo Gu, Zhengyi |
author_sort | Liu, Chong |
collection | PubMed |
description | Ischemic heart disease is a leading cause of mortality and morbidity worldwide. We previously demonstrated that acacetin protects against myocardial ischemia reperfusion injury in rats, although the underlying mechanism remains to be elucidated. In the present study, we investigated the effects of acacetin on autophagy during hypoxia/reoxygenation (H/R) injury by exposing H9c2 myocardial cells to H/R with or without acacetin pretreatment during hypoxia. Our results show that acacetin significantly increased cell viability in a dose-dependent manner, enhanced antioxidant capacity, and suppressed protein apoptosis of rat cardiomyocytes H9c2 cells following H/R injury. In addition, lentiviral infection of H9c2 cardiomyocytes revealed that acacetin pretreatment significantly enhanced the fluorescence intensity of autophagy proteins Beclin 1, LC3-II, and p62. These results indicate that acacetin protected H9c2 cardiomyocytes from H/R damage by enhancing autophagy. Moreover, we found that application of acacetin increased activation of the PI3K/Akt signaling pathway, whereas cotreatment with the PI3K inhibitor LY294002 reversed the inhibition of apoptosis and autophagy induced by acacetin. In conclusion, acacetin mitigated H/R injury by promoting autophagy through activating the PI3K/Akt/mTOR signaling pathway. |
format | Online Article Text |
id | pubmed-8263275 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-82632752021-07-22 Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy Liu, Chong Zhang, Minmin Ye, Shenyi Hong, Chenliang Chen, Jiaxi Lu, Ruyue Hu, Bingjie Yang, Weijun Shen, Bo Gu, Zhengyi J Immunol Res Research Article Ischemic heart disease is a leading cause of mortality and morbidity worldwide. We previously demonstrated that acacetin protects against myocardial ischemia reperfusion injury in rats, although the underlying mechanism remains to be elucidated. In the present study, we investigated the effects of acacetin on autophagy during hypoxia/reoxygenation (H/R) injury by exposing H9c2 myocardial cells to H/R with or without acacetin pretreatment during hypoxia. Our results show that acacetin significantly increased cell viability in a dose-dependent manner, enhanced antioxidant capacity, and suppressed protein apoptosis of rat cardiomyocytes H9c2 cells following H/R injury. In addition, lentiviral infection of H9c2 cardiomyocytes revealed that acacetin pretreatment significantly enhanced the fluorescence intensity of autophagy proteins Beclin 1, LC3-II, and p62. These results indicate that acacetin protected H9c2 cardiomyocytes from H/R damage by enhancing autophagy. Moreover, we found that application of acacetin increased activation of the PI3K/Akt signaling pathway, whereas cotreatment with the PI3K inhibitor LY294002 reversed the inhibition of apoptosis and autophagy induced by acacetin. In conclusion, acacetin mitigated H/R injury by promoting autophagy through activating the PI3K/Akt/mTOR signaling pathway. Hindawi 2021-06-29 /pmc/articles/PMC8263275/ /pubmed/34307696 http://dx.doi.org/10.1155/2021/9979843 Text en Copyright © 2021 Chong Liu 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 Liu, Chong Zhang, Minmin Ye, Shenyi Hong, Chenliang Chen, Jiaxi Lu, Ruyue Hu, Bingjie Yang, Weijun Shen, Bo Gu, Zhengyi Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy |
title | Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy |
title_full | Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy |
title_fullStr | Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy |
title_full_unstemmed | Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy |
title_short | Acacetin Protects Myocardial Cells against Hypoxia-Reoxygenation Injury through Activation of Autophagy |
title_sort | acacetin protects myocardial cells against hypoxia-reoxygenation injury through activation of autophagy |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8263275/ https://www.ncbi.nlm.nih.gov/pubmed/34307696 http://dx.doi.org/10.1155/2021/9979843 |
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