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Sevoflurane preconditioning protects experimental ischemic stroke by enhancing anti‐inflammatory microglia/macrophages phenotype polarization through GSK‐3β/Nrf2 pathway
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Sevoflurane preconditioning protects experimental ischemic stroke by enhancing anti‐inflammatory microglia/macrophages phenotype polarization through GSK‐3β/Nrf2 pathway
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Sevoflurane preconditioning protects experimental ischemic stroke by enhancing anti‐inflammatory microglia/macrophages phenotype polarization through GSK‐3β/Nrf2 pathway
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Journal Article
Sevoflurane preconditioning protects experimental ischemic stroke by enhancing anti‐inflammatory microglia/macrophages phenotype polarization through GSK‐3β/Nrf2 pathway
2021
Overview
Aims Sevoflurane preconditioning (SPC) results in cerebral ischemic tolerance; however, the mechanism remains unclear. Promoting microglia/macrophages polarization from pro‐inflammatory state to anti‐inflammatory phenotype has been indicated as a potential treatment target against ischemic stroke. In this study, we aimed to assess the effect of SPC on microglia polarization after stroke and which signaling pathway was involved in this transition. Methods Mouse primary microglia with SPC were challenged by oxygen‐glucose deprivation (OGD) or lipopolysaccharide (LPS), and mice with SPC were subjected to middle cerebral artery occlusion (MCAO). Then, the mRNA and protein levels of pro‐inflammatory/anti‐inflammatory factors were analyzed. GSK‐3β phosphorylation and Nrf2 nuclear translocation were measured. The mRNA and protein expression of pro‐inflammatory/anti‐inflammatory factors, neurological scores, infarct volume, cellular apoptosis, the proportion of pro‐inflammatory/anti‐inflammatory microglia/macrophages, and the generation of super‐oxidants were examined after SPC or GSK‐3β inhibitor TDZD treatment with or without Nrf2 deficiency. Results Sevoflurane preconditioning promoted anti‐inflammatory and inhibited pro‐inflammatory microglia/macrophages phenotype both in vitro and in vivo. GSK‐3β phosphorylation at Ser9 was increased after SPC. Both SPC and TDZD administration enhanced Nrf2 nuclear translocation, reduced pro‐inflammatory microglia/macrophages markers expression, promoted anti‐inflammatory markers level, and elicited a neuroprotective effect. Nrf2 deficiency abolished the promoted anti‐inflammatory microglia/macrophages polarization and ischemic tolerance induced by TDZD treatment. The reduced percentage of pro‐inflammatory positive cells and super‐oxidants generation induced by SFC or TDZD was also reversed by Nrf2 knockdown. Conclusions Our results indicated that SPC exerts brain ischemic tolerance and promotes anti‐inflammatory microglia/macrophages polarization by GSK‐3β‐dependent Nrf2 activation, which provides a novel mechanism for SPC‐induced neuroprotection. SPC promoted microglia/macrophages polarization toward to anti‐inflammatory phenotype in vitro and in vivo. Both SPC and TDZD administration enhanced Nrf2 nuclear translocation.SPC promoted microglia/macrophages toward to anti‐inflammatory phenotype shifting via GSK‐3β‐dependent Nrf2 activation.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
Subject
Anesthetics, Inhalation - therapeutic use
/ Animals
/ Enzymes
/ Glycogen Synthase Kinase 3 beta - antagonists & inhibitors
/ Glycogen Synthase Kinase 3 beta - drug effects
/ glycogen synthesis kinase‐3β
/ Infarction, Middle Cerebral Artery - pathology
/ Ischemia
/ Ischemic Stroke - prevention & control
/ Kinases
/ Male
/ Mice
/ microglia/macrophages phenotype shift
/ mRNA
/ Neuroinflammatory Diseases - drug therapy
/ Neuroinflammatory Diseases - pathology
/ Neuroprotective Agents - therapeutic use
/ NF-E2-Related Factor 2 - antagonists & inhibitors
/ NF-E2-Related Factor 2 - drug effects
/ nuclear factor erythroid 2–related factor
/ Original
/ Oxidants
/ Proteins
/ Sevoflurane - therapeutic use
/ Signal Transduction - drug effects
/ Stroke
