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Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury

Growing evidence demonstrated that cell death pathways including ferroptosis, apoptosis and necroptosis contribute to cardiac ischaemia/reperfusion (I/R) injury. We hypothesized that ferroptosis, apoptosis and necroptosis contribute differently to myocardial damage during acute cardiac I/R injury. R...

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Autores principales: Luo, Ying, Apaijai, Nattayaporn, Liao, Suchan, Maneechote, Chayodom, Chunchai, Titikorn, Arunsak, Busarin, Benjanuwattra, Juthipong, Yanpiset, Panat, Chattipakorn, Siriporn C., Chattipakorn, Nipon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8995446/
https://www.ncbi.nlm.nih.gov/pubmed/35315192
http://dx.doi.org/10.1111/jcmm.17275
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author Luo, Ying
Apaijai, Nattayaporn
Liao, Suchan
Maneechote, Chayodom
Chunchai, Titikorn
Arunsak, Busarin
Benjanuwattra, Juthipong
Yanpiset, Panat
Chattipakorn, Siriporn C.
Chattipakorn, Nipon
author_facet Luo, Ying
Apaijai, Nattayaporn
Liao, Suchan
Maneechote, Chayodom
Chunchai, Titikorn
Arunsak, Busarin
Benjanuwattra, Juthipong
Yanpiset, Panat
Chattipakorn, Siriporn C.
Chattipakorn, Nipon
author_sort Luo, Ying
collection PubMed
description Growing evidence demonstrated that cell death pathways including ferroptosis, apoptosis and necroptosis contribute to cardiac ischaemia/reperfusion (I/R) injury. We hypothesized that ferroptosis, apoptosis and necroptosis contribute differently to myocardial damage during acute cardiac I/R injury. Rats underwent cardiac I/R or sham operation. I/R‐operated rats were divided into 4 groups: vehicle, apoptosis (Z‐vad), ferroptosis (Fer‐1) and necroptosis (Nec‐1) inhibition. Rats in each cell death inhibitor group were subdivided into 3 different dose regimens: low, medium and high. Infarct size, left ventricular (LV) function, arrhythmias and molecular mechanism were investigated. Cardiac I/R caused myocardial infarction, LV dysfunction, arrhythmias, mitochondrial dysfunction, mitochondrial dynamic imbalance, inflammation, apoptosis and ferroptosis. Infarct size, LV dysfunction, mitochondrial dysfunction, apoptosis and ferroptosis were all reduced to a similar extent in rats treated with Z‐vad (low and medium doses) or Fer‐1 (medium and high doses). Fer‐1 treatment also reduced mitochondrial dynamic imbalance and inflammation. No evidence of necroptosis was found in association with acute I/R injury, therefore Nec‐1 treatment could not be assessed. Apoptosis and ferroptosis, not necroptosis, contributed to myocardial damage in acute I/R injury. Inhibitors of these 2 pathways provided effective cardioprotection in rats with I/R injury though modulation of mitochondrial function and attenuated apoptosis and ferroptosis.
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spelling pubmed-89954462022-04-15 Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury Luo, Ying Apaijai, Nattayaporn Liao, Suchan Maneechote, Chayodom Chunchai, Titikorn Arunsak, Busarin Benjanuwattra, Juthipong Yanpiset, Panat Chattipakorn, Siriporn C. Chattipakorn, Nipon J Cell Mol Med Original Articles Growing evidence demonstrated that cell death pathways including ferroptosis, apoptosis and necroptosis contribute to cardiac ischaemia/reperfusion (I/R) injury. We hypothesized that ferroptosis, apoptosis and necroptosis contribute differently to myocardial damage during acute cardiac I/R injury. Rats underwent cardiac I/R or sham operation. I/R‐operated rats were divided into 4 groups: vehicle, apoptosis (Z‐vad), ferroptosis (Fer‐1) and necroptosis (Nec‐1) inhibition. Rats in each cell death inhibitor group were subdivided into 3 different dose regimens: low, medium and high. Infarct size, left ventricular (LV) function, arrhythmias and molecular mechanism were investigated. Cardiac I/R caused myocardial infarction, LV dysfunction, arrhythmias, mitochondrial dysfunction, mitochondrial dynamic imbalance, inflammation, apoptosis and ferroptosis. Infarct size, LV dysfunction, mitochondrial dysfunction, apoptosis and ferroptosis were all reduced to a similar extent in rats treated with Z‐vad (low and medium doses) or Fer‐1 (medium and high doses). Fer‐1 treatment also reduced mitochondrial dynamic imbalance and inflammation. No evidence of necroptosis was found in association with acute I/R injury, therefore Nec‐1 treatment could not be assessed. Apoptosis and ferroptosis, not necroptosis, contributed to myocardial damage in acute I/R injury. Inhibitors of these 2 pathways provided effective cardioprotection in rats with I/R injury though modulation of mitochondrial function and attenuated apoptosis and ferroptosis. John Wiley and Sons Inc. 2022-03-21 2022-04 /pmc/articles/PMC8995446/ /pubmed/35315192 http://dx.doi.org/10.1111/jcmm.17275 Text en © 2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Luo, Ying
Apaijai, Nattayaporn
Liao, Suchan
Maneechote, Chayodom
Chunchai, Titikorn
Arunsak, Busarin
Benjanuwattra, Juthipong
Yanpiset, Panat
Chattipakorn, Siriporn C.
Chattipakorn, Nipon
Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury
title Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury
title_full Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury
title_fullStr Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury
title_full_unstemmed Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury
title_short Therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury
title_sort therapeutic potentials of cell death inhibitors in rats with cardiac ischaemia/reperfusion injury
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8995446/
https://www.ncbi.nlm.nih.gov/pubmed/35315192
http://dx.doi.org/10.1111/jcmm.17275
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