Dexamethasone enhances NT-3 expression in rat hippocampus after traumatic brain injury |
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| Authors: | Jen-Tsung Yang Tsong-Hai Lee Hsu-Huei Weng Chen-Nen Chang Wen-Cheng Chen Wan-Chun Cheng June Hsieh Wu |
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| Affiliation: | a Departments of Neurosurgery, Chang Gung Memorial Hospital, Chia-Yi, Taiwan;b Departments of Neurology, Chang Gung Memorial Hospital, Taipei, Taiwan;c Departments of Radiology, Chang Gung Memorial Hospital, Chia-Yi, Taiwan;d Departments of Neurosurgery, Chang Gung Memorial Hospital, Taipei, Taiwan;e Departments of Radiation Oncology, Chang Gung Memorial Hospital, Chia-Yi, Taiwan;f Departments of Neurosurgery, Tsu-Ai General Hospital, Shi-Luo, Taiwan;g Molecular Genetics Laboratory 3, College of Medicine, Chang Gung University, 259 Wen Hwa I Road, Kwei-San, Tao-Yuan 333, Taiwan |
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| Abstract: | The cellular events in traumatic brain injury (TBI) are complicated, and the factors mediating neurotrophins to protect and repair the injured brain cells are only beginning to be identified. This study examined the effect of dexamethasone (DEX) on neurotrophin-3 (NT-3) expression following TBI. Levels of NT-3 mRNA and protein in rat hippocampus were measured using in situ hybridization and immunohistochemistry, respectively. After TBI, the NT-3 mRNA expression was down-regulated during the first 24 h. DEX reversed the post-traumatic reduction of NT-3 mRNA expression at 2, 4, 6, and 12 h in the hippocampus, and also decreased the cell death in hippocampal hilum and supraventricular cerebral cortex after 7 days. The NT-3 protein levels generally corresponded to the mRNA levels in the hippocampal region. DEX enhanced the NT-3 expression after TBI, indicating that post-traumatic neuroprotection in the hippocampus is at least partially mediated by NT-3 and thus can be modulated by DEX treatment. |
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| Keywords: | Dexamethasone Hippocampus In situ hybridization Immunohistochemistry Neurotrophin-3 Traumatic brain injury |
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