Journal
NEUROMOLECULAR MEDICINE
Volume 19, Issue 4, Pages 541-554Publisher
HUMANA PRESS INC
DOI: 10.1007/s12017-017-8468-4
Keywords
IL-17; TBI; Secondary brain injury; Inflammation; IL-23/IL-17 axis
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Funding
- National Natural Science Foundation of China [81271267]
- 333 Program'' of Jiangsu Province [BRA2015068]
- Jiangsu social development or Natural Science Foundation [BE2016645, BK20161153, BK20161171, BE2017641]
- Xuzhou Natural Science Foundation [KC15J0060, KC15SX009]
- Jiangsu Educational Science Foundation [KJS1410]
- Jiangsu Provincial Commission of Health and Family Planning, Genera Programs [H201527]
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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.
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