中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (10): 1660-1665.doi: 10.4103/1673-5374.193247

• 原著:周围神经损伤修复保护与再生 • 上一篇    下一篇

硼酸可减轻损伤坐骨神经的轴突和髓鞘损害

  

  • 收稿日期:2016-10-08 出版日期:2016-10-31 发布日期:2016-10-31

Boric acid reduces axonal and myelin damage in experimental sciatic nerve injury

Zahir Kızılay1, *, Haydar Ali Erken2, Nesibe Kahraman Çetin3, Serdar Aktaş4, Burçin İrem Abas5, Ali Yılmaz1   

  1. 1 Department of Neurosurgery, Faculty of Medicine, Adnan Menderes University, Aydin, Turkey 2 Department of Physiology, Faculty of Medicine, Balikesir University, Balikesir, Turkey 3 Department of Pathology, Faculty of Medicine, Adnan Menderes University, Aydin, Turkey 4 Department of Pharmacology and Toxicology, Faculty of Medicine, Adnan Menderes University, Aydin, Turkey 5 Department of Clinical Biochemistry, Faculty of Medicine, Adnan Menderes University, Aydin, Turkey
  • Received:2016-10-08 Online:2016-10-31 Published:2016-10-31
  • Contact: Zahir Kizilay, M.D., zahir.kizilay@adu.edu.tr.

PDF

288

摘要：

为研究硼酸对坐骨神经损伤的影响，实验设计将28只成年雄性大鼠随机等分为4组：对照组、硼酸干预治疗组、坐骨神经损伤组和坐骨神经损伤+硼酸治疗组。对照组大鼠不损伤坐骨神经，不给予硼酸灌胃；坐骨神经损伤组只应用动脉瘤夹夹伤坐骨神经，未灌胃硼酸；坐骨神经损伤+硼酸干预治疗组在大鼠坐骨神经动脉瘤夹夹伤后0，24，48，72h分4次以100 mg/kg剂量灌胃硼酸；硼酸干预治疗组大鼠在对应4个时间灌胃硼酸，但未损伤坐骨神经。电生理和坐骨神经组织HE和甲苯胺蓝染色检测显示，相较于对照组和硼酸干预治疗组，坐骨神经损伤组大鼠在实验第4天，损伤坐骨神经复合动作电位和神经传导速度及轴突数量明显下降，髓鞘结构遭到破坏。坐骨神经损伤+硼酸干预治疗组大鼠在实验第4天，损伤坐骨神经电生理功能、轴突数量、髓鞘结构的破坏程度均较坐骨神经损伤组明显改善，轴突和许旺细胞中核因子B的免疫反应较坐骨神经损伤明显降低。说明100 mg/kg硼酸可减轻坐骨神经轴突和髓鞘结构形态损害，并改变损伤坐骨神经的电生理功能，该作用可能与减轻氧化反应有关。 

orcid: 0000-0002-2021-0406 (Zahir Kizilay)

关键词: 神经再生, 周围神经损伤, 坐骨神经, 硼酸, 神经传导, 轴突, 髓鞘, 电生理

Abstract: Te aim of this study was to investigate the e?ects of boric acid in experimental acute sciatic nerve injury. Twenty-eight adult male rats were randomly divided into four equal groups (n = 7): control (C), boric acid (BA), sciatic nerve injury (I) , and sciatic nerve injury + boric acid treatment (BAI). Sciatic nerve injury was generated using a Yasargil aneurysm clip in the groups I and BAI. Boric acid was given four times at 100 mg/kg to rats in the groups BA and BAI afer injury (by gavage at 0, 24, 48 and 72 hours) but no injury was made in the group BA. In vivo electrophysiological tests were performed at the end of the day 4 and sciatic nerve tissue samples were taken for histopathological examination. The amplitude of compound action potential, the nerve conduction velocity and the number of axons were signifcantly lower and the myelin structure was found to be broken in group I compared with those in groups C and BA. However, the amplitude of the compound action potential, the nerve conduction velocity and the number of axons were signifcantly greater in group BAI than in group I. Moreover, myelin injury was signifcantly milder and the intensity of nuclear factor kappa B immunostaining was signifcantly weaker in group BAI than in group I. Te results of this study show that administration of boric acid at 100 mg/kg afer sciatic nerve injury in rats markedly reduces myelin and axonal injury and improves the electrophysiological function of injured sciatic nerve possibly through alleviating oxidative stress reactions.

Key words: nerve regeneration, peripheral nerve injury, sciatic nerve, boric acid, nerve conduction velocity, axon, myelin, electrophysiology, neural regeneration