中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (5): 540-548.doi: 10.4103/1673-5374.130096

• 原著:周围神经损伤修复保护与再生 • 上一篇    下一篇

预先压挫配合脊神经根拔除会增加运动神经元存活率

  

  • 收稿日期:2014-01-08 出版日期:2014-03-12 发布日期:2014-03-12
  • 基金资助:

    江苏省教育厅项目(编号:08KJB310002)| 江苏省优势学科项目(编号:JX10131801096)

Preconditioning crush increases the survival rate of motor neurons after spinal root avulsion

Lin Li, Yizhi Zuo, Jianwen He   

  1. Department of Human Anatomy, Nanjing Medical University, Nanjing, Jiangsu Province, China
  • Received:2014-01-08 Online:2014-03-12 Published:2014-03-12
  • Contact: Jianwen He, M.D., Department of Human Anatomy, Nanjing Medical University, Nanjing 210029, Jiangsu Province, China, jianghe6562@163.com.
  • Supported by:

    This study was supported by a grant from Education Ministry of Jiangsu Province, No. 08KJB310002; Excellent Discipline of Jiangsu Province, No. JX10131801096.

摘要:

以往研究表明,在脊神经根拔除或压挫后,腹侧运动神经元中的热休克蛋白27持续上调,热休克蛋白27的上调是否会增加运动神经元的存活率?鉴于此,实验将大鼠分为2组:单纯拔除组只对第4腰神经进行拔除,拔除前预先压挫组在对第4腰神经根拔除前1周对其压挫。免疫荧光染色结果表明:与单纯拔除组相比,拔除前预先压挫组的运动神经元的存活率明显提高,这种提高一直持续到拔除后直到第5周。和这种存活率提高相关的是:在拔除前预先压挫组的运动神经元中热休克蛋白27的表达也是增加的。与此相形成对照的是:在预先压挫组的运动神经元中的一氧化氮合酶的表达是显著下降,而一氧化氮合酶所产生的一氧化氮在运动神经元损伤中起到毒性作用。实验结果提示:预先压挫所导致的神经保护机制可能是通过增加热休克蛋白27的上调和减弱一氧化氮合酶上调而起作用的。

关键词: 神经再生, 神经根性撕脱伤, 脊神经根, 热休克蛋白27, 一氧化氮合酶, 运动神经元, 荧光抗体技术, 胆碱乙酰转移酶

Abstract:

In a previous study, heat shock protein 27 was persistently upregulated in ventral motor neurons following nerve root avulsion or crush. Here, we examined whether the upregulation of heat shock protein 27 would increase the survival rate of motor neurons. Rats were divided into two groups: an avulsion-only group (avulsion of the L4 lumbar nerve root only) and a crush-avulsion group (the L4 lumbar nerve root was crushed 1 week prior to the avulsion). Immunofluorescent staining revealed that the survival rate of motor neurons was significantly greater in the crush-avulsion group than in the avulsion-only group, and this difference remained for at least 5 weeks after avulsion. The higher neuronal survival rate may be explained by the upregulation of heat shock protein 27 expression in motor neurons in the crush-avulsion group. Furthermore, preconditioning crush greatly attenuated the expression of nitric oxide synthase in the motor neurons. Our findings indicate that the neuroprotective action of preconditioning crush is mediated through the upregulation of heat shock protein 27 expression and the attenuation of neuronal nitric oxide synthase upregulation following avulsion.

Key words: nerve regeneration, nerve root avulsion, spinal nerve root, heat shock protein 27, nitric oxide synthase, motor neurons, fluorescent antibody technique, choline acetyltransferase, a grant from Education Ministry of Jiangsu Province, Excellent Discipline of Jiangsu Province, neural regeneration