Dural Functions of Brain-Derived Neurotrofic Factor (BDNF) in Compression-Induced Spinal Cord Injury

神经营养因子增强神经系统中细胞在生理和病理条件下的存活，例如由疾病或创伤引起的那些。我们用脊髓受压损伤的大鼠证明了BDNF的两种不同功能。通过对铜锌超氧化物歧化酶（SOD）表达的影响评价其保护神经元和胶质细胞的功能，通过对髓鞘碱性蛋白（MBP）表达的影响评价其促进轴突再生的功能。脊髓压迫伤后24 h内SOD表达下调，随后恢复。BDNF可抑制SOD表达的下调并促进其恢复。MBP表达在损伤后立即大大降低。BDNF治疗缓解了其急性下降，并促进其在2周后逐渐增加。值得注意的是，BDNF对轴突再生的促进作用在BDNF给药停止后保持。这项动物研究为BDNF在人类脊髓损伤中的潜在临床应用提供了数据支持。

Neurotrophins enhance the survival of cells in the nervous system under both physiological and pathological conditions, such as those caused by diseases or trauma. We demonstrated two distinct functions of BDNF using rats that had received compression-induced spinal cord injury. Its function in protecting neurons and glia was evaluated by its effects on Cu Zn superoxide dismutase (SOD) expression, and its function in promoting axonal regeneration was assessed by its effects on myelin basic protein (MBP) expression. SOD expression in the spinal cord was down-regulated within 24 h of compression-induced injury and then recovered. BDNF inhibited the down-regulation of SOD expression and accelerated its recovery. MBP expression was immediately and greatly reduced after injury. BDNF administration relieved its acute decrease and promoted its gradual increase after 2 weeks. It is notable that the facilitating effect of BDNF on the axonal regeneration was maintained after cessation of BDNF administration. This animal study provides data supporting the potential clinical application of BDNF in human spinal cord injury.