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TLR5 Activation through NF-kappa B Is a Neuroprotective Mechanism of Postconditioning after Cerebral Ischemia in Mice

Authors
Jeong, JaewonKim, SoojinLim, Da-SolKim, Seo-HeaDoh, HeejuKim, So-DamSong, Yun Seon
Issue Date
Aug-2017
Publisher
KOREAN SOC BRAIN & NEURAL SCIENCE, KOREAN SOC NEURODEGENERATIVE DISEASE
Keywords
Neuroprotection; Postconditioning; Cerebral ischemia; Toll-like receptor 5; Nuclear factor kappa B
Citation
EXPERIMENTAL NEUROBIOLOGY, v.26, no.4, pp 213 - 226
Pages
14
Journal Title
EXPERIMENTAL NEUROBIOLOGY
Volume
26
Number
4
Start Page
213
End Page
226
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8218
DOI
10.5607/en.2017.26.4.213
ISSN
1226-2560
2093-8144
Abstract
Postconditioning has been shown to protect the mouse brain from ischemic injury. However, the neuroprotective mechanisms of postconditioning remain elusive. We have found that toll-like receptor 5 (TLR5) plays an integral role in postconditioning-induced neuroprotection through Akt/nuclear factor kappa B (NF-kappa B) activation in cerebral ischemia. Compared to animals that received 30 min of transient middle cerebral artery occlusion (tMCAO) group, animals that also underwent postconditioning showed a significant reduction of up to 60.51% in infarct volume. Postconditioning increased phospho-Akt (p-Akt) levels and NF-kappa B translocation to the nucleus as early as 1 h after tMCAO and oxygen-glucose deprivation. Furthermore, inhibition of Akt by Akt inhibitor IV decreased NF-kappa B promoter activity after postconditioning. Immunoprecipitation showed that interactions between TLR5, MyD88, and p-Akt were increased from postconditioning both in vivo and in vitro. Similar to postconditioning, flagellin, an agonist of TLR5, increased NF-kappa B nuclear translocation and Akt phosphorylation. Our results suggest that postconditioning has neuroprotective effects by activating NF-kappa B and Akt survival pathways via TLR5 after cerebral ischemia. Additionally, the TLR5 agonist flagellin can simulate the neuroprotective mechanism of postconditioning in cerebral ischemia.
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