Su Huanxing, Yuan Qiuju, Qin Dajiang, Yang Xiaoying, Wong Wai-Man, So Kwok-Fai, Wu Wutian
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau.
Department of Anatomy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong.
Biomed Res Int. 2014;2014:658753. doi: 10.1155/2014/658753. Epub 2014 May 20.
Brachial plexus injury often involves traumatic root avulsion resulting in permanent paralysis of the innervated muscles. The lack of sufficient regeneration from spinal motoneurons to the peripheral nerve (PN) is considered to be one of the major causes of the unsatisfactory outcome of various surgical interventions for repair of the devastating injury. The present study was undertaken to investigate potential inhibitory signals which influence axonal regeneration after root avulsion injury. The results of the study showed that root avulsion triggered GSK-3β activation in the injured motoneurons and remaining axons in the ventral funiculus. Systemic application of a clinical dose of lithium suppressed activated GSK-3β in the lesioned spinal cord to the normal level and induced extensive axonal regeneration into replanted ventral roots. Our study suggests that GSK-3β activity is involved in negative regulation for axonal elongation and regeneration and lithium, the specific GSK-3β inhibitor, enhances motoneuron regeneration from CNS to PNS.
臂丛神经损伤常涉及创伤性神经根撕脱，导致受其支配的肌肉永久性麻痹。脊髓运动神经元向周围神经（PN）的再生不足被认为是各种修复严重损伤的外科手术效果不尽人意的主要原因之一。本研究旨在探究影响神经根撕脱损伤后轴突再生的潜在抑制信号。研究结果表明，神经根撕脱会触发损伤运动神经元和脊髓腹侧索中剩余轴突的糖原合成酶激酶-3β（GSK-3β）激活。临床剂量锂的全身应用可将损伤脊髓中激活的GSK-3β抑制至正常水平，并诱导大量轴突再生至重新植入的腹侧神经根。我们的研究表明，GSK-3β活性参与轴突伸长和再生的负调控，而锂这种特定的GSK-3β抑制剂可增强运动神经元从中枢神经系统（CNS）到周围神经系统（PNS）的再生。
