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Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway
To determine whether sevoflurane postconditioning protects against cerebral ischemia reperfusion (I/R) injury and its potential mechanism, we employed bioinformatic analysis, neurological assessments, and western blot analysis, as well as triphenyl tetrazolium chloride, hematoxylin and eosin, Nissl,...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9831726/ https://www.ncbi.nlm.nih.gov/pubmed/36585924 http://dx.doi.org/10.18632/aging.204461 |
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author | Zhao, Zijun Li, Yishuai Chi, Fei Ma, Li Li, Yanan Hou, Zhiyong Wang, Qiujun |
author_facet | Zhao, Zijun Li, Yishuai Chi, Fei Ma, Li Li, Yanan Hou, Zhiyong Wang, Qiujun |
author_sort | Zhao, Zijun |
collection | PubMed |
description | To determine whether sevoflurane postconditioning protects against cerebral ischemia reperfusion (I/R) injury and its potential mechanism, we employed bioinformatic analysis, neurological assessments, and western blot analysis, as well as triphenyl tetrazolium chloride, hematoxylin and eosin, Nissl, and immunofluorescence staining. We identified 103 differentially expressed genes induced by cerebral I/R, including 75 upregulated genes and 28 downregulated genes enriched for certain biological processes (involving regulation of inflammatory responses, cellular responses to interleukin 1, and chemokine activity) and signaling pathways (such as transcriptional misregulation in cancer, interleukin-17 signaling, rheumatoid arthritis, MAPK signaling, and Toll-like receptor signaling). As a typical path in Toll-like receptor signaling pathway, in the current study, we investigated the protective effect of sevoflurane postconditioning in cerebral I/R rats and further explore the role of TLR4/MyD88/TRAF6 signaling pathway in it. The results showed cerebral I/R-induced neurological deficits were comparatively less severe following sevoflurane postconditioning. In addition, TLR4/MyD88/TRAF6 signaling pathway-related proteins and neuropathic damage were ameliorated in aged rats following sevoflurane postconditioning, while the TLR4 agonist lipopolysaccharide aggravated these changes. Together, these findings suggest that sevoflurane postconditioning ameliorates cerebral I/R injury by a mechanism involving inhibition of the TLR4/MyD88/TRAF6 signaling pathway to suppress neuroinflammatory responses. |
format | Online Article Text |
id | pubmed-9831726 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-98317262023-01-11 Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway Zhao, Zijun Li, Yishuai Chi, Fei Ma, Li Li, Yanan Hou, Zhiyong Wang, Qiujun Aging (Albany NY) Research Paper To determine whether sevoflurane postconditioning protects against cerebral ischemia reperfusion (I/R) injury and its potential mechanism, we employed bioinformatic analysis, neurological assessments, and western blot analysis, as well as triphenyl tetrazolium chloride, hematoxylin and eosin, Nissl, and immunofluorescence staining. We identified 103 differentially expressed genes induced by cerebral I/R, including 75 upregulated genes and 28 downregulated genes enriched for certain biological processes (involving regulation of inflammatory responses, cellular responses to interleukin 1, and chemokine activity) and signaling pathways (such as transcriptional misregulation in cancer, interleukin-17 signaling, rheumatoid arthritis, MAPK signaling, and Toll-like receptor signaling). As a typical path in Toll-like receptor signaling pathway, in the current study, we investigated the protective effect of sevoflurane postconditioning in cerebral I/R rats and further explore the role of TLR4/MyD88/TRAF6 signaling pathway in it. The results showed cerebral I/R-induced neurological deficits were comparatively less severe following sevoflurane postconditioning. In addition, TLR4/MyD88/TRAF6 signaling pathway-related proteins and neuropathic damage were ameliorated in aged rats following sevoflurane postconditioning, while the TLR4 agonist lipopolysaccharide aggravated these changes. Together, these findings suggest that sevoflurane postconditioning ameliorates cerebral I/R injury by a mechanism involving inhibition of the TLR4/MyD88/TRAF6 signaling pathway to suppress neuroinflammatory responses. Impact Journals 2022-12-29 /pmc/articles/PMC9831726/ /pubmed/36585924 http://dx.doi.org/10.18632/aging.204461 Text en Copyright: © 2022 Zhao et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Zhao, Zijun Li, Yishuai Chi, Fei Ma, Li Li, Yanan Hou, Zhiyong Wang, Qiujun Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway |
title | Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway |
title_full | Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway |
title_fullStr | Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway |
title_full_unstemmed | Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway |
title_short | Sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via TLR4/MyD88/TRAF6 signaling pathway |
title_sort | sevoflurane postconditioning ameliorates cerebral ischemia-reperfusion injury in rats via tlr4/myd88/traf6 signaling pathway |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9831726/ https://www.ncbi.nlm.nih.gov/pubmed/36585924 http://dx.doi.org/10.18632/aging.204461 |
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