Citation

Li T, Zhang YM, Han D, Hua R, Guo BN, Hu SQ, Yan XL, Xu T. Neuromolecular Med. 2017; 19(4): 541-554.

Affiliation

Emergency Center of the Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, China. xutie889@163.com.

Copyright

(Copyright © 2017, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s12017-017-8468-4

PMID

28916896

Abstract

The pro-inflammatory activity of interleukin 17, which is produced by the IL-23/IL-17 axis, has been associated with the pathogenesis of traumatic brain injury (TBI). The study investigated the potential role of IL-17 in secondary brain injury of TBI in a rat model. Our data showed that the levels of IL-17 increased from 6 h to 7 days and peaked at 3 days, in both the CNS and serum, which were consistent with the severity of secondary brain injury. The IL-23 inhibitor suberoylanilide hydroxamic acid (SAHA) treatment markedly decreased the expressions of IL-17 and apoptosis-associated proteins cleaved caspase-3 and increased the protein ratio of Bcl-2 (B cell lymphoma/leukemia-2)/Bax (Bcl-2-associated X protein). Meanwhile, neuronal apoptosis was reduced, and neural function was improved after SAHA treatment. This study suggests that IL-17 is involved in secondary brain injury after TBI. Administering an IL-23 inhibitor and thereby blocking the IL-23/IL-17 axis may be beneficial in the treatment of TBI.

Language: en

Keywords

IL-17; IL-23/IL-17 axis; Inflammation; Secondary brain injury; TBI