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Exp Neurobiol. 2017 Aug;26(4):213-226. doi: 10.5607/en.2017.26.4.213. Epub 2017 Aug 28.

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

Experimental neurobiology

Jaewon Jeong, Soojin Kim, Da-Sol Lim, Seo-Hea Kim, Heeju Doh, So-Dam Kim, Yun Seon Song

Affiliations

  1. College of Pharmacy, Sookmyung Women's University, Seoul 04310, Korea.

PMID: 28912644 PMCID: PMC5597552 DOI: 10.5607/en.2017.26.4.213

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-κB) 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-κB 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-κB promoter activity after postconditioning. Immunoprecipitation showed that interactions between TLR5, MyD88, and p-Akt were increased from postconditioning both

Keywords: Cerebral ischemia; Neuroprotection; Nuclear factor kappa B; Postconditioning; Toll-like receptor 5

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