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Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway

Although reperfusion of the ischemic myocardium has been used as a vital treatment of various patients with cardiovascular disease, the accompanying myocardial ischemia-reperfusion injury (MIRI) can cause further damage, resulting in a poor prognosis. The present study aimed to explore the roles and...

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Autores principales: Li, Yuanyuan, Wang, Zhongyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9366315/
https://www.ncbi.nlm.nih.gov/pubmed/35978933
http://dx.doi.org/10.3892/etm.2022.11504
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author Li, Yuanyuan
Wang, Zhongyan
author_facet Li, Yuanyuan
Wang, Zhongyan
author_sort Li, Yuanyuan
collection PubMed
description Although reperfusion of the ischemic myocardium has been used as a vital treatment of various patients with cardiovascular disease, the accompanying myocardial ischemia-reperfusion injury (MIRI) can cause further damage, resulting in a poor prognosis. The present study aimed to explore the roles and regulatory mechanisms of interleukin (IL)-32, a pro-inflammatory cytokine, in MIRI. Cardiomyocytes were subjected to hypoxia and reoxygenation (H/R) to mimic MIRI. The effects of IL-32 on oxidative stress, inflammation and apoptosis of H/R-treated cells were assessed. Given that the nucleotide-binding oligomerization domain 2 (NOD2) and NADPH oxidase 2 (NOX2) play roles in the inflammatory response and myocardial ischemia, the role of this regulatory axis in the function of IL-32 was evaluated. The results indicated that IL-32 levels were elevated following H/R treatment. Downregulation of IL-32 expression attenuated H/R-induced reduction in cell viability, LDH release, oxidative stress, inflammation and apoptosis. Moreover, downregulation of IL-32 expression reversed the activation of the NOD2/NOX2/MAPK signaling pathway caused by H/R treatment. NOD2 overexpression altered the effects of the downregulation of IL-32 expression on the cells, indicating that this regulatory axis mediated the function of IL-32. Collectively, the data indicated that IL-32 participated in the induction of oxidative stress, inflammation, and apoptosis in cardiomyocytes during H/R treatment via the NOD2/NOX2/MAPK signaling pathway.
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spelling pubmed-93663152022-08-16 Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway Li, Yuanyuan Wang, Zhongyan Exp Ther Med Articles Although reperfusion of the ischemic myocardium has been used as a vital treatment of various patients with cardiovascular disease, the accompanying myocardial ischemia-reperfusion injury (MIRI) can cause further damage, resulting in a poor prognosis. The present study aimed to explore the roles and regulatory mechanisms of interleukin (IL)-32, a pro-inflammatory cytokine, in MIRI. Cardiomyocytes were subjected to hypoxia and reoxygenation (H/R) to mimic MIRI. The effects of IL-32 on oxidative stress, inflammation and apoptosis of H/R-treated cells were assessed. Given that the nucleotide-binding oligomerization domain 2 (NOD2) and NADPH oxidase 2 (NOX2) play roles in the inflammatory response and myocardial ischemia, the role of this regulatory axis in the function of IL-32 was evaluated. The results indicated that IL-32 levels were elevated following H/R treatment. Downregulation of IL-32 expression attenuated H/R-induced reduction in cell viability, LDH release, oxidative stress, inflammation and apoptosis. Moreover, downregulation of IL-32 expression reversed the activation of the NOD2/NOX2/MAPK signaling pathway caused by H/R treatment. NOD2 overexpression altered the effects of the downregulation of IL-32 expression on the cells, indicating that this regulatory axis mediated the function of IL-32. Collectively, the data indicated that IL-32 participated in the induction of oxidative stress, inflammation, and apoptosis in cardiomyocytes during H/R treatment via the NOD2/NOX2/MAPK signaling pathway. D.A. Spandidos 2022-07-12 /pmc/articles/PMC9366315/ /pubmed/35978933 http://dx.doi.org/10.3892/etm.2022.11504 Text en Copyright: © Li et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Yuanyuan
Wang, Zhongyan
Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway
title Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway
title_full Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway
title_fullStr Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway
title_full_unstemmed Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway
title_short Interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the NOD2/NOX2/MAPK signaling pathway
title_sort interleukin 32 participates in cardiomyocyte-induced oxidative stress, inflammation and apoptosis during hypoxia/reoxygenation via the nod2/nox2/mapk signaling pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9366315/
https://www.ncbi.nlm.nih.gov/pubmed/35978933
http://dx.doi.org/10.3892/etm.2022.11504
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