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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,...

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Autores principales: Zhao, Zijun, Li, Yishuai, Chi, Fei, Ma, Li, Li, Yanan, Hou, Zhiyong, Wang, Qiujun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2022
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.
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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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