@article{ref1,
title="Involvement of IL-17 in secondary brain injury after a traumatic brain injury in rats",
journal="Neuromolecular medicine",
year="2017",
author="Li, Tan and Zhang, Yong-Mei and Han, Dong and Hua, Rong and Guo, Bing-Nan and Hu, Shu-Qun and Yan, Xian-Liang and Xu, Tie",
volume="19",
number="4",
pages="541-554",
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.<p /> <p>Language: en</p>",
language="en",
issn="1535-1084",
doi="10.1007/s12017-017-8468-4",
url="http://dx.doi.org/10.1007/s12017-017-8468-4"
}