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Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy
Myocardial diseases are prevalent syndromes with high mortality rate. The exploration of effective interference is important. Anti-β1-adrenergic receptor autoantibody (β1-AAB) is highly correlated with myocardial dysfunction. The actions and underlying mechanisms of honokiol (HNK) in β1-AAB-positive...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6079338/ https://www.ncbi.nlm.nih.gov/pubmed/30116474 http://dx.doi.org/10.1155/2018/1640804 |
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author | Wei, Xi-qing Zhang, Hong-sheng Wei, Guang-he Zhang, Jin-guo Du, Yan-yan Tan, Hong-yong Yang, Jun |
author_facet | Wei, Xi-qing Zhang, Hong-sheng Wei, Guang-he Zhang, Jin-guo Du, Yan-yan Tan, Hong-yong Yang, Jun |
author_sort | Wei, Xi-qing |
collection | PubMed |
description | Myocardial diseases are prevalent syndromes with high mortality rate. The exploration of effective interference is important. Anti-β1-adrenergic receptor autoantibody (β1-AAB) is highly correlated with myocardial dysfunction. The actions and underlying mechanisms of honokiol (HNK) in β1-AAB-positive patients await to be unraveled. In this study, we established a rat model of β1-AAB positive with myocardial dysfunction. Cardiac function following β1-AR-ECII administration was analyzed using the VisualSonics Vevo 770 High-Resolution In Vivo Imaging System. The levels of autophagy-related proteins were detected by Western blotting. Our data revealed that HNK reversed β1-AAB-induced effects and protected myocardial tissues from dysfunction. After HNK treatment, the cardiac contractile ability increased and the LDH activity decreased. HNK attenuated myocardial degeneration. In addition, HNK promoted the activation of the AMP-dependent protein kinase/Unc-51-like autophagy activating kinase (AMPK/ULK) pathway and activated autophagy. These results suggest that HNK protects against β1-AAB-induced myocardial dysfunction via activation of autophagy and it may be a potentially therapeutic compound for β1-AAB-positive myocardial diseases. |
format | Online Article Text |
id | pubmed-6079338 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-60793382018-08-16 Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy Wei, Xi-qing Zhang, Hong-sheng Wei, Guang-he Zhang, Jin-guo Du, Yan-yan Tan, Hong-yong Yang, Jun Oxid Med Cell Longev Research Article Myocardial diseases are prevalent syndromes with high mortality rate. The exploration of effective interference is important. Anti-β1-adrenergic receptor autoantibody (β1-AAB) is highly correlated with myocardial dysfunction. The actions and underlying mechanisms of honokiol (HNK) in β1-AAB-positive patients await to be unraveled. In this study, we established a rat model of β1-AAB positive with myocardial dysfunction. Cardiac function following β1-AR-ECII administration was analyzed using the VisualSonics Vevo 770 High-Resolution In Vivo Imaging System. The levels of autophagy-related proteins were detected by Western blotting. Our data revealed that HNK reversed β1-AAB-induced effects and protected myocardial tissues from dysfunction. After HNK treatment, the cardiac contractile ability increased and the LDH activity decreased. HNK attenuated myocardial degeneration. In addition, HNK promoted the activation of the AMP-dependent protein kinase/Unc-51-like autophagy activating kinase (AMPK/ULK) pathway and activated autophagy. These results suggest that HNK protects against β1-AAB-induced myocardial dysfunction via activation of autophagy and it may be a potentially therapeutic compound for β1-AAB-positive myocardial diseases. Hindawi 2018-07-18 /pmc/articles/PMC6079338/ /pubmed/30116474 http://dx.doi.org/10.1155/2018/1640804 Text en Copyright © 2018 Xi-qing Wei et al. http://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 Wei, Xi-qing Zhang, Hong-sheng Wei, Guang-he Zhang, Jin-guo Du, Yan-yan Tan, Hong-yong Yang, Jun Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy |
title | Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy |
title_full | Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy |
title_fullStr | Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy |
title_full_unstemmed | Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy |
title_short | Honokiol Protects against Anti-β1-Adrenergic Receptor Autoantibody-Induced Myocardial Dysfunction via Activation of Autophagy |
title_sort | honokiol protects against anti-β1-adrenergic receptor autoantibody-induced myocardial dysfunction via activation of autophagy |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6079338/ https://www.ncbi.nlm.nih.gov/pubmed/30116474 http://dx.doi.org/10.1155/2018/1640804 |
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