中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (1): 163-167.doi: 10.4103/1673-5374.175064

• 原著:周围神经损伤修复保护与再生 • 上一篇    下一篇

地塞米松可能对周围神经非冻结性冷损伤具有早期缓解作用

  

  • 收稿日期:2015-08-14 出版日期:2016-01-15 发布日期:2016-01-15
  • 基金资助:

     四川省医学会“施慧达”科研课题(SHD12-21);宜宾市卫生局医学科研项目

Dexamethasone prevents vascular damage in early-stage non-freezing cold injury of the sciatic nerve

Hao Li 1, Lei Zhang 2, Min Xu 3   

  1. 1 Department of Neurology, the First People’s Hospital of Yibin, Yibin, Sichuan Province, China
    2 Department of Pharmacy, the First People’s Hospital of Yibin, Yibin, Sichuan Province, China
    3 Department of Neurology, Xuanwu Hospital Capital Medical University, Beijing, China
  • Received:2015-08-14 Online:2016-01-15 Published:2016-01-15
  • Contact: Hao Li, lihao_1981@163.com.
  • Supported by:

    This study was supported by grants from “Shihuida” Scientific Research Program of Sichuan Province Medical Association of China, No. SHD12-21; and Medical Scientific Research Program of Health Bureau of Yibin City in China.

摘要:

糖皮质激素具有的抗炎和抑制损伤部位脂质过氧化反应的作用,是否可能对周围神经非冻结性冷损伤产生治疗效应?实验给予雄性Wistar大鼠一侧坐骨神经以3-5 ℃持续低温2 h建立非冻结性冷损伤模型,以腹腔注射3 mg/kg地塞米松进行治疗。发现冷损伤1d时坐骨神经中示踪剂伊文思蓝浓度明显下降,神经内膜未见伊文思蓝明显渗出,神经内膜中的毛细血管腔未见狭窄,但有髓纤维仍有严重退变。地塞米松干预坐骨神经非冻结性冷损伤后,神经内膜血管病变得到明显改善,但有髓纤维病变并未缓解,提示地塞米松可能保护血-神经屏障,但对冷损伤的治疗作用可能仅限于血管系统。

关键词: 神经再生, 周围神经损伤, 坐骨神经, 低温, 血-神经屏障, 非冻结性冷损伤, 地塞米松

Abstract:

Non-freezing cold injury is a prevalent cause of peripheral nerve damage, but its pathogenic mechanism is poorly understood, and treatment
remains inadequate. Glucocorticoids have anti-inflammatory and lipid peroxidation-inhibiting properties. We therefore examined whether dexamethasone, a synthetic glucocorticoid compound, would alleviate early-stage non-freezing cold injury of the sciatic nerve. We established Wistar rat models of non-freezing cold injury by exposing the left sciatic nerve to cold (3–5°C) for 2 hours, then administered dexamethasone (3 mg/kg intraperitoneally) to half of the models. One day after injury, the concentration of Evans blue tracer in the injured sciatic nerve of rats that received dexamethasone was notably lower than that in the injured sciatic nerve of rats that did not receive dexamethasone; neither Evans blue dye nor capillary stenosis was observed in the endoneurium, but myelinated nerve fibers were markedly degenerated in the injured sciatic nerve of animals that received dexamethasone. After dexamethasone administration, however, endoneurial vasculopathy was markedly improved, although damage to the myelinated nerve fiber was not alleviated. These findings suggest that dexamethasone protects the blood-nerve barrier, but its benefit in non-freezing cold injury is limited to the vascular system.

Key words: nerve regeneration, peripheral nerve injury, sciatic nerve, hypothermia, blood-nerve barrier, non-freezing cold injury, dexamethasone, neural regeneration