中国神经再生研究(英文版) ›› 2016, Vol. 11 ›› Issue (4): 525-528.doi: 10.4103/1673-5374.180724

• 综述:神经损伤修复保护与再生 •    下一篇

亲水性聚合物:促进轴突融合的一种新技术

  

  • 收稿日期:2016-02-26 出版日期:2016-04-30 发布日期:2016-04-30
  • 基金资助:

    这项工作由美国国防部OR120216资助。

A novel technique using hydrophilic polymers to promote axonal fusion

Ravinder Bamba1, 2, *, D. Colton Riley1, 3, Nathaniel D. Kelm4, Mark D. Does4, Richard D. Dortch5, Wesley P. Thayer1   

  1. 1 Department of Plastic Surgery, Vanderbilt University Medical Center, Nashville, TN, USA
    2 Department of Surgery, Georgetown University, Washington, DC, USA
    3 Georgetown University School of Medicine, Washington, DC, USA
    4 Vanderbilt University Institute of Imaging Science, Nashville, TN, USA
    5 Department of Radiology and Radiological Sciences, Vanderbilt University, Nashville, TN, USA
  • Received:2016-02-26 Online:2016-04-30 Published:2016-04-30
  • Contact: Ravinder Bamba, M.D., Ravinder.bamba@vanderbilt.edu.
  • Supported by:

    This work was supported by the Department of Defense: Grant Number OR120216--Development of Class II Medical Device for Clinical Translation of a Novel PEG Fusion Method for Immediate Physiological Recovery after Peripheral Nerve Injury.

摘要:

神经损伤不是致命的,但会严重影响生活质量。周围神经损伤发生通常会造成上肢创伤。周围神经损伤的预后不佳,主要是由于轴突生长的过程缓慢。神经损伤后,完好细胞体切断的近端轴突生长速度可以达到1毫米/天。再生轴突优先靶向适当的终末器官受体,但也并不总能直接生长至标靶。由于生长缓慢和运动感觉神经纤维的错乱排列,功能恢复效果也并不尽如人意。肌肉失神经支配后肌肉萎缩会立即发生,如果运动轴突没有在一个关键的时间窗口内达到它们的目标肌肉,肌组织是不太容易接受时神经重新支配的。
最常见的周围神经修复策略主要包括脱细胞同种异体神经移植,组织基质和神经生长导向技术,从而促进轴突再生,并减轻周围炎症。然而,缓慢的轴突生长,沃勒变性,肌肉萎缩的组合是阻碍功能恢复的最大障碍。文章主要应用聚乙二醇,一种令人兴奋的技术来促进轴突融合,从而显著提高轴突再生,并加强神经再支配。他们采用聚乙二醇在钙离子游离状态下与传统的神经修复相结合,来实现神经切断后的立即修复以及轴突融合,但不导致沃勒变性,是促进周围神经损伤后轴突融合的新技术。

orcid: 0000-0002-5432-2764 (Ravinder Bamba)

Abstract:

The management of traumatic peripheral nerve injury remains a considerable concern for clinicians. With
minimal innovations in surgical technique and a limited number of specialists trained to treat peripheral
nerve injury, outcomes of surgical intervention have been unpredictable. The inability to manipulate the
pathophysiology of nerve injury (i.e., Wallerian degeneration) has left scientists and clinicians depending
on the slow and lengthy process of axonal regeneration (~1 mm/day). When axons are severed, the endings
undergo calcium-mediated plasmalemmal sealing, which limits the ability of the axon to be primarily repaired.
Polythethylene glycol (PEG) in combination with a bioengineered process overcomes the inability
to fuse axons. The mechanism for PEG axonal fusion is not clearly understood, but multiple studies have
shown that a providing a calcium-free environment is essential to the process known as PEG fusion. The
proposed mechanism is PEG-induced lipid bilayer fusion by removing the hydration barrier surrounding
the axolemma and reducing the activation energy required for membrane fusion to occur. This review
highlights PEG fusion, its past and current studies, and future directions in PEG fusion.

Key words: peripheral nerve injury, polyethylene glycol, axonal fusion, nerve transection, traumatic neuropathy