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Sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation

Brain ischemia causes irreversible damage to functional neurons in cases of infarct. Promoting endogenous neurogenesis to replace necrotic neurons is a promising therapeutic strategy for ischemia patients. The neuroprotective role of sevoflurane preconditioning implies that it might also enhance end...

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Autores principales: Li, Li, Saiyin, Hexige, Xie, Jingmo, Ma, Lixiang, Xue, Lei, Wang, Wei, Liang, Weimin, Yu, Qiong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438671/
https://www.ncbi.nlm.nih.gov/pubmed/28212538
http://dx.doi.org/10.18632/oncotarget.15325
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author Li, Li
Saiyin, Hexige
Xie, Jingmo
Ma, Lixiang
Xue, Lei
Wang, Wei
Liang, Weimin
Yu, Qiong
author_facet Li, Li
Saiyin, Hexige
Xie, Jingmo
Ma, Lixiang
Xue, Lei
Wang, Wei
Liang, Weimin
Yu, Qiong
author_sort Li, Li
collection PubMed
description Brain ischemia causes irreversible damage to functional neurons in cases of infarct. Promoting endogenous neurogenesis to replace necrotic neurons is a promising therapeutic strategy for ischemia patients. The neuroprotective role of sevoflurane preconditioning implies that it might also enhance endogenous neurogenesis and functional restoration in the infarct region. By using a transient middle cerebral artery occlusion (tMCAO) model, we discovered that endogenous neurogenesis was enhanced by sevoflurane preconditioning. This enhancement process is characterized by the promotion of neuroblast proliferation within the subventricular zone (SVZ), migration and differentiation into neurons, and the presence of astrocytes and oligodendrocytes at the site of infarct. The newborn neurons in the sevoflurane preconditioning group showed miniature excitatory postsynaptic currents (mEPSCs), increased synaptophysin and PSD95 staining density, indicating normal neuronal function. Furthermore, long-term behavioral improvement was observed in the sevoflurane preconditioning group consistent with endogenous neurogenesis. Further histological analyses showed that sevoflurane preconditioning accelerated microglial activation, including migration, phagocytosis and secretion of brain-derived neurotrophic factor (BDNF). Intraperitoneal injection of minocycline, a microglial inhibitor, suppressed microglial activation and reversed neurogenesis. Our data showed that sevoflurane preconditioning promoted microglial activities, created a favorable microenvironment for endogenous neurogenesis and accelerated functional reconstruction in the infarct region.
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spelling pubmed-54386712017-05-24 Sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation Li, Li Saiyin, Hexige Xie, Jingmo Ma, Lixiang Xue, Lei Wang, Wei Liang, Weimin Yu, Qiong Oncotarget Research Paper Brain ischemia causes irreversible damage to functional neurons in cases of infarct. Promoting endogenous neurogenesis to replace necrotic neurons is a promising therapeutic strategy for ischemia patients. The neuroprotective role of sevoflurane preconditioning implies that it might also enhance endogenous neurogenesis and functional restoration in the infarct region. By using a transient middle cerebral artery occlusion (tMCAO) model, we discovered that endogenous neurogenesis was enhanced by sevoflurane preconditioning. This enhancement process is characterized by the promotion of neuroblast proliferation within the subventricular zone (SVZ), migration and differentiation into neurons, and the presence of astrocytes and oligodendrocytes at the site of infarct. The newborn neurons in the sevoflurane preconditioning group showed miniature excitatory postsynaptic currents (mEPSCs), increased synaptophysin and PSD95 staining density, indicating normal neuronal function. Furthermore, long-term behavioral improvement was observed in the sevoflurane preconditioning group consistent with endogenous neurogenesis. Further histological analyses showed that sevoflurane preconditioning accelerated microglial activation, including migration, phagocytosis and secretion of brain-derived neurotrophic factor (BDNF). Intraperitoneal injection of minocycline, a microglial inhibitor, suppressed microglial activation and reversed neurogenesis. Our data showed that sevoflurane preconditioning promoted microglial activities, created a favorable microenvironment for endogenous neurogenesis and accelerated functional reconstruction in the infarct region. Impact Journals LLC 2017-02-14 /pmc/articles/PMC5438671/ /pubmed/28212538 http://dx.doi.org/10.18632/oncotarget.15325 Text en Copyright: © 2017 Li et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Li, Li
Saiyin, Hexige
Xie, Jingmo
Ma, Lixiang
Xue, Lei
Wang, Wei
Liang, Weimin
Yu, Qiong
Sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation
title Sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation
title_full Sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation
title_fullStr Sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation
title_full_unstemmed Sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation
title_short Sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation
title_sort sevoflurane preconditioning induced endogenous neurogenesis against ischemic brain injury by promoting microglial activation
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5438671/
https://www.ncbi.nlm.nih.gov/pubmed/28212538
http://dx.doi.org/10.18632/oncotarget.15325
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