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Exp Neurobiol 2017; 26(4): 213-226
Published online August 31, 2017
https://doi.org/10.5607/en.2017.26.4.213
© The Korean Society for Brain and Neural Sciences
Jaewon Jeong, Soojin Kim, Da-Sol Lim, Seo-Hea Kim, Heeju Doh, So-Dam Kim and Yun Seon Song*
College of Pharmacy, Sookmyung Women’s University, Seoul 04310, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-2077-7231, FAX: 82-2-710-9871
e-mail: yssong@sookmyung.ac.kr
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: Neuroprotection, Postconditioning, Cerebral ischemia, Toll-like receptor 5, Nuclear factor kappa B