Electrical stimulation promotes regeneration of defective peripheral nerves after delayed repair intervals lasting under one month.
Electrical stimulation promotes regeneration of defective peripheral nerves after delayed repair intervals lasting under one month.
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延迟修复间隔持续不到一个月后，电刺激可促进有缺陷的周围神经的再生
DOI：
10.1371/journal.pone.0105045
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Jiang B
中科院分区：
文献类型：
--
作者：
Xu C;Kou Y;Zhang P;Han N;Yin X;Deng J;Chen B;Jiang B
背景电刺激（ES）已被证明是提高神经再生速度和准确性的有效手段。然而，这些结果是在神经损伤后几乎立即进行手术时记录的。在临床环境中，大多数患者不能立即得到治疗。一些严重创伤或污染伤口的患者需要等待神经修复手术。延迟神经修复已被证明与立即手术相比结果较差。目前尚不清楚在足够长的时间后，电刺激是否仍然对神经再生有任何影响。方法建立大鼠延迟神经修复模型，分别于术后1天、1周、1个月、2个月进行延迟神经修复。在每个时间点，用可吸收导管桥接一半大鼠的神经残端，并给予大鼠1 h的弱电刺激。另一半则未接受治疗。为了分析这些组之间的形态学和分子差异，在手术后5天每个时间点处死6只ES大鼠和6只假ES大鼠。每组中的其他大鼠在最终功能测试和组织观察之前允许恢复6周。结果ES大鼠和假ES大鼠远端神经残端有髓纤维数量均随修复延迟时间的延长而减少。延迟1天和延迟1周组，ES大鼠的纤维比假ES大鼠多。两组ES大鼠的复合肌肉动作电位（CMAP）和运动神经传导速度（MNCV）均优于对照组。为了分析这些差异背后的机制，对远端神经进行Masson染色，对脊髓进行定量PCR。结果表明，延迟修复1个月和2个月后，所有大鼠的远端神经均出现较多的胶原组织增生。脑源性神经营养因子（BDNF）和trkB在ES大鼠脊髓中的表达水平高于假ES大鼠。然而，这些差异随着修复延迟的增加而减少。结论电刺激不能持续促进神经修复后的长时间延迟。延迟修复后神经再生的有效时间小于1个月。其作用机制可能与神经生长因子的表达和神经再生环境有关。
Background Electrical stimulation (ES) has been proven to be an effective means of enhancing the speed and accuracy of nerve regeneration. However, these results were recorded when the procedure was performed almost immediately after nerve injury. In clinical settings, most patients cannot be treated immediately. Some patients with serious trauma or contaminated wounds need to wait for nerve repair surgery. Delays in nerve repair have been shown to be associated with poorer results than immediate surgery. It is not clear whether electrical stimulation still has any effect on nerve regeneration after enough time has elapsed. Methods A delayed nerve repair model in which the rats received delayed nerve repair after 1 day, 1 week, 1 month, and 2 months was designed. At each point in time, the nerve stumps of half the rats were bridged with an absorbable conduit and the rats were given 1 h of weak electrical stimulation. The other half was not treated. In order to analyze the morphological and molecular differences among these groups, 6 ES rats and 6 sham ES rats per point in time were killed 5 days after surgery. The other rats in each group were allowed to recover for 6 weeks before the final functional test and tissue observation. Results The amounts of myelinated fibers in the distal nerve stumps decreased as the delay in repair increased for both ES rats and sham ES rats. In the 1-day-delay and 1-week-delay groups, there were more fibers in ES rats than in sham ES rats. And the compound muscle action potential (CMAP) and motor nerve conduction velocity (MNCV) results were better for ES rats in these two groups. In order to analyze the mechanisms underlying these differences, Masson staining was performed on the distal nerves and quantitative PCR on the spinal cords. Results showed that, after delays in repair of 1 month and 2 months, there was more collagen tissue hyperplasia in the distal nerve in all rats. The brain-derived neurotrophic factor (BDNF) and trkB expression levels in the spinal cords of ES rats were higher than in sham ES rats. However, these differences decreased as the delay in repair increased. Conclusions Electrical stimulation does not continue to promote nerve regeneration after long delays in nerve repair. The effective interval for nerve regeneration after delayed repair was found to be less than 1 month. The mechanism seemed to be related to the expression of nerve growth factors and regeneration environment in the distal nerves.
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影响因子：
2.3
作者：
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