中国神经再生研究(英文版) ›› 2014, Vol. 9 ›› Issue (10): 1055-1062.doi: 10.4103/1673-5374.133170

• 原著:周围神经损伤修复保护与再生 • 上一篇    下一篇

足底切开大鼠脊神经元钠钾氯联合转运蛋白1和钾氯联合转运蛋白2的变化及鞘内布美他尼的镇痛作用

  

  • 收稿日期:2014-03-10 出版日期:2014-05-26 发布日期:2014-05-26
  • 基金资助:

    广州医学院科研基金项目(2008C24)

Analgesic effect of intrathecal bumetanide is accompanied by changes in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain

Yanbing He 1, 2, Shiyuan Xu 1, Junjie Huang 2, Qingjuan Gong 2   

  1. 1 Department of Anesthesiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China
    2 Department of Anesthesiology and Pain Medicine, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong Province, China
  • Received:2014-03-10 Online:2014-05-26 Published:2014-05-26
  • Contact: Shiyuan Xu, M.D., Department of Anesthesiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong Province, China, xushiyuan355@163.com.
  • Supported by:

    This study was supported by a grant from Guangzhou Medical University, No. 2008C24.

摘要:

以往研究显示,钠钾氯联合转运蛋白1和钾氯联合转运蛋白2,可通过调节疼痛通路神经元的氯离子浓度影响神经元兴奋性和疼痛敏化,从而参与了脊髓水平的疼痛传导的调控。实验假设布美他尼的镇痛效应是通过钠钾氯联合转运蛋白1和钾氯联合转运蛋白2的作用途径而表达得。实验结果显示,在鞘内注射布美他尼使足底切开模型大鼠的痛感降低,热痛阈及机械痛阈提高;荧光免疫染色检测到未注射布美他尼的足底切开模型大鼠脊髓双侧背根节和同侧背角深层神经元的钠钾氯联合转运蛋白1表达增加,同侧背角深层神经元的钾氯联合转运蛋白2表达降低。结果证实,足底切割损伤后脊髓神经元钠钾氯联合转运蛋白1表达上调,钾氯联合转运蛋白2表达下调,鞘内注射布美他尼过抑制钠钾氯联合转运蛋白1的功能而镇痛。

关键词: 神经再生, 钠钾氯联合转运蛋白1, 钾氯联合转运蛋白2, 布美他尼, 脊髓, 背根神经节, 切割, 术后痛, 广州医学院科研基金

Abstract:

Accumulating evidence has demonstrated that the sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 have a role in the modulation of pain transmission at the spinal level through chloride regulation in the pain pathway and by effecting neuronal excitability and pain sensitization. The present study aimed to investigate the analgesic effect of the specific sodium-potassium-chloride co-transporter 1 inhibitor bumetanide, and the change in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain. Results showed that intrathecal bumetanide could decrease cumulative pain scores, and could increase thermal and mechanical pain thresholds in a rat model of incisional pain. Sodium-potassium-chloride co-transporter 1 expression increased in neurons from dorsal root ganglion and the deep laminae of the ipsilateral dorsal horn following incision. By contrast, potassium-chloride co-transporter 2 expression decreased in neurons of the deep laminae from the ipsilateral dorsal horn. These findings suggest that spinal sodium-potassium-chloride co-transporter 1 expression was up-regulated and spinal potassium-chloride co-transporter 2 expression was down-regulated following incision. Intrathecal bumetanide has analgesic effects on incisional pain through inhibition of sodium-potassium-chloride co-transporter 1.

Key words: nerve regeneration, sodium-potassium-chloride co-transporter 1, potassium-chloride co-transporter 2, bumetanide, spinal cord, dorsal root ganglion, incision model, postoperative pain, neural regeneration