1. IL-17 potentiates neuronal injury induced by oxygen-glucose deprivation and affects neuronal IL-17 receptor expression.
- Author
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Wang DD, Zhao YF, Wang GY, Sun B, Kong QF, Zhao K, Zhang Y, Wang JH, Liu YM, Mu LL, Wang DS, and Li HL
- Subjects
- Animals, Apoptosis, Cells, Cultured, Hippocampus pathology, Humans, Interleukin-17 analysis, Interleukin-17 genetics, Male, Mice, Mice, Inbred C57BL, Receptors, Interleukin-17 analysis, Receptors, Interleukin-17 genetics, Brain Ischemia pathology, Cell Hypoxia, Glucose metabolism, Interleukin-17 physiology, Neurons pathology, Receptors, Interleukin-17 physiology
- Abstract
Interleukin-17 (IL-17) is active in a variety of brain injuries, including ischemia. The objective of this study was to test the hypothesis that IL-17 potentiates neuronal injury after stroke. Increased expression of IL-17 and IL-17 receptor (IL-17R) in serum and cortex was evaluated by ELISA, RT-PCR and immunohistochemistry. In the in vitro model of oxygen-glucose deprivation (OGD), IL-17 showed a dose-dependent effect in promoting neuronal injury through IL-17-IL-17R combination which can be blocked by IL-17R/Fc chimera. Our results demonstrated the up-regulation of IL-17 and IL-17R following permanent middle cerebral artery occlusion and suggested that they contributed to stroke outcome.
- Published
- 2009
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