中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (2): 309-316.doi: 10.4103/1673-5374.226401

• 原著:周围神经损伤修复保护与再生 • 上一篇    下一篇

损伤神经吻合口包裹壳聚糖-二丙酸倍他米松缓释膜：促进周围神经再生效果更好？

  

  • 收稿日期:2017-11-05 出版日期:2018-02-15 发布日期:2018-02-15

Anastomotic stoma coated with chitosan film as a betamethasone dipropionate carrier for peripheral nerve regeneration

Ping Yao1, Peng Li2, Jun-jian Jiang3, Hong-ye Li4   

  1. 1 Department of Hand Surgery, Hangzhou Plastic Surgery Hospital, Hangzhou, Zhejiang Province, China
    2 Department of Anesthesia, Affiliated Puai Hospital of Huazhong University of Science and Technology, Wuhan, Hubei Province, China
    3 Department of Hand Surgery, Huashan Hospital, Fudan University, Shanghai, China
    4 Department of Hand Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China
  • Received:2017-11-05 Online:2018-02-15 Published:2018-02-15
  • Contact: Jun-jian Jiang, M.D., Ph.D. or Hong-ye Li, jjjdoctor@126.com or swrhxy@yeah.net.

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摘要：

阻碍周围神经损伤吻合修复效果的重要原因是神经缝合口局部的瘢痕增生，为解决此问题，目前常采用两种修复方法，一种为利用一些生物制剂阻隔神经缝合口和周围组织以达到物理防粘连的效果，利用一些甾体类激素如抑制炎症反应的药理作用以达到防止瘢痕增生，但促进损伤神经再生的总体效果均不满意。为此，我们设想能将此2种方法相结合，取长补短，以达到更好的神经修复效果。实验在大鼠取右股后部斜切口，在胫神经入腓肠肌前的1.0 cm外切断，建立胫神经损伤大鼠模型。神经切断后直接缝合，然后在吻合口包裹5 cm ?5 cm 的壳聚糖-二丙酸倍他米松缓释膜。损伤后12周，与单独神经切断后直接缝合及神经切断后直接缝合联合吻合口涂抹聚乳酸的模型大鼠相比，壳聚糖-二丙酸倍他米松缓释膜在模型大鼠体内降解缓慢，膜形态仍保持完整，损伤神经吻合口局部瘢痕增生和粘连程度明显减轻，再生神经纤维结构较完整，排列整齐，电生理检查可见损伤神经复合肌肉动作电位增强。结果可证实壳聚糖-二丙酸倍他米松缓释膜能有效防止胫神经修复后局部瘢痕的增生，促进神经的再生。

orcid:0000-0001-6087-1308(Jun-jian Jiang)
          0000-0001-9823-1277(Hong-ye Li)

 

关键词: 壳聚糖, 二丙酸倍他米松, 神经再生, 瘢痕, 神经损伤, 修复, 功能恢复, 膜, 药物释放, 载体

Abstract:

Scar hyperplasia at the suture site is an important reason for hindering the repair effect of peripheral nerve injury anastomosis. To address this issue, two repair methods are often used. Biological agents are used to block nerve sutures and the surrounding tissue to achieve physical anti-adhesion effects. Another agent is glucocorticosteroid, which can prevent scar growth by inhibiting inflammation. However, the overall effect of promoting regeneration of the injured nerve is not satisfactory. In this regard, we envision that these two methods can be combined and lead to shared understanding for achieving improved nerve repair. In this study, the right tibial nerve was transected 1 cm above the knee to establish a rat tibial nerve injury model. The incision was directly sutured after nerve transection. The anastomotic stoma was coated with 0.5 × 0.5 cm2 chitosan sheets with betamethasone dipropionate. At 12 weeks after injury, compared with the control and poly (D, L-lactic acid) groups, chitosan-betamethasone dipropionate film slowly degraded with the shape of the membrane still intact. Further, scar hyperplasia and the degree of adhesion at anastomotic stoma were obviously reduced, while the regenerated nerve fiber structure was complete and arranged in a good order in model rats. Electrophysiological study showed enhanced compound muscle action potential. Our results confirm that chitosan-betamethasone dipropionate film can effectively prevent local scar hyperplasia after tibial nerve repair and promote nerve regeneration.

Key words: nerve regeneration, chitosan, betamethasone dipropionate, scar, nerve injury, repair, function restoration, film, drug release, carrier, neural regeneration