中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (10): 1851-1855.doi: 10.3969/j.issn.1673-8225.2012.10.031

• 干细胞移植 stem cell transplantation • 上一篇    下一篇

坐骨神经损伤大鼠模型鞘内移植神经干细胞后脊髓背角和背根神经节脑源性神经营养因子的表达★

张民皓1,胡益民1,张  红2,胡玉萍1,刘清珍1,王洪超2,李伟彦1   

  1. 1解放军南京军区南京总医院麻醉科,江苏省南京市 210002;2徐州医学院江苏省麻醉学重点实验室,江苏省徐州市 221002
  • 收稿日期:2011-09-09 修回日期:2011-12-27 出版日期:2012-03-04 发布日期:2012-03-04
  • 通讯作者: 李伟彦,主任医师,教授,博士,硕士生导师,解放军南京军区南京总医院麻醉科,江苏省南京市 210002 weiyanlee@yahoo.com.cn
  • 作者简介:张民皓★,男,1984年生,江苏省南京市人,汉族,徐州医学院在读硕士,主要从事疼痛诊疗的研究。daxiang0077@163.com

Brain-derived neurotrophic factor expression in the spinal dorsal horn and dorsal root ganglion in a rat model of sciatic nerve injury after intrathecal transplantation of neural stem cells 

Zhang Min-hao1, Hu Yi-min1, Zhang Hong2, Hu Yu-ping1, Liu Qing-zhen1, Wang Hong-chao2, Li Wei-yan1   

  1. 1Department of Anesthesiology, Nanjing General Hospital of Nanjing Military Command, PLA, Nanjing 210002, Jiangsu Province, China; 2Key Laboratory of Anesthesiology of Jiangsu Province, Xuzhou Medical College, Xuzhou 221002, Jiangsu Province, China
  • Received:2011-09-09 Revised:2011-12-27 Online:2012-03-04 Published:2012-03-04
  • Contact: author: Li Wei-yan, M.D., Chief physician, Professor, Master’s supervisor, Department of Anesthesiology, Nanjing General Hospital of Nanjing Military Command, PLA, Nanjing 210002, Jiangsu Province, China
  • About author:Zhang Min-hao★, Studying for master’s degree, Key Laboratory of Anesthesiology of Jiangsu Province, Xuzhou Medical College, Xuzhou 221002, Jiangsu Province, China daxiang0077@163.com

摘要:

背景:坐骨神经损伤模型可测试伤害性的热刺激和机械刺激所引发的痛觉过敏及冷、触觉异常。
目的:观察坐骨神经损伤模型大鼠鞘内移植神经干细胞后脊髓背角和背根神经节脑源性神经营养因子的表达。
方法:72只SD大鼠随机均分为假手术组、对照组和实验组。对照组和实验组制作坐骨神经损伤模型,假手术组仅暴露坐骨神经,不结扎。分别于造模后第3,10天进行鞘内移植,实验组注入30 μL的神经干细胞悬液,空白组和对照组注入30 μL的细胞培养液。
结果与结论:与假手术组相比,对照组和实验组移植后3 d机械痛阈和热痛阈逐渐降低,至移植后7 d降低至最低点(P < 0.01),于移植后21 d恢复至移植前水平;实验组移植后7,14 d机械痛阈和热痛阈较对照组明显上升(P < 0.01)。与对照组相比,假手术组移植后7,14,21 d各组大鼠脑源性神经营养因子的表达呈低水平(P < 0.05);移植后14,21 d,实验组脑源性神经营养因子的表达量高于对照组(P < 0.05)。提示鞘内移植神经干细胞可提高脊髓背角和背根神经节中脑源性神经营养因子的表达。从而抑制了周围神经损伤产生的神经病理性疼痛。
关键词:脑源性神经营养因子;神经干细胞;慢性限制损伤;脊髓背角;背根神经节
doi:10.3969/j.issn.1673-8225.2012.10.031

关键词: 脑源性神经营养因子, 神经干细胞, 慢性限制损伤, 脊髓背角, 背根神经节

Abstract:

BACKGROUND: The model of sciatic nerve injury can be used to test the hyperalgesia and paraesthesia caused by nocuous heat stimulation and mechanical stimulation.
OBJECTIVE: To investigate the expression of brain-derived neurotrophic factor (BDNF) in the spinal dorsal horn and dorsal root ganglion in a rat model of sciatic nerve injury after intrathecal transplantation of neural stem cells.
METHODS: Seventy-two adult Sprague-Dawley rats were randomly divided into sham-operation, control and experimental groups. Rat model of sciatic nerve injury was established in the control and experimental groups. In the sham-operation group, only sciatic nerve was exposed, without ligation. Intratheal transplantation was performed at 3 and 10 days after induction of sciatic nerve injury. 30 μL of neural stem cell suspension was injected into the experimental group, and 30 μL cell culture solution was injected into the sham-operation and control groups.  
RESULTS AND CONCLUSION: Compared with sham-operation group, mechanical withdrawal threshold and thermal withdrawal latency were gradually reduced at 3 days after transplantation, decreased to the lowest level at 7 days (P < 0.01) and recovered to pre-transplantation level at 21 days in the control and experimental groups. At 7 and 14 days after transplantation, mechanical withdrawal threshold and thermal withdrawal latency were significantly increased in the experimental group than in the control group (P < 0.01). Compared with control group, at 7, 14 and 21 days after transplantation, BDNF expression was significantly decreased in the experimental group (P < 0.05). At 14 and 21 days after transplantation, BDNF expression was significantly higher in the experimental group than in the control group (P < 0.05). These findings show that intrathecal transplantation of neural stem cells can prevent and treat the neuropathic pain from peripheral nerve injury by increasing BDNF expression in the spinal dorsal horn and dorsal root ganglion.

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