Kosins Aaron M, Scholz Thomas, Lin Michael, Evans Gregory R D, Keirstead Hans S
Reeve-Irvine Research Center, Irvine, CA, USA.
Ann Plast Surg. 2012 Mar;68(3):290-4. doi: 10.1097/SAP.0b013e31823dce7e.
Our recent experiments demonstrate that demyelination enhances peripheral nerve regeneration after contusion injury in the adult rat sciatic nerve. The role of demyelination in peripheral nerve regeneration in a sciatic nerve transection model has yet to be elucidated. We hypothesize that (1) axon regeneration within a region of injury increases after experimental, immunologic demyelination, and (2) regenerated axons are partially derived from the proximal motor axons.
Sciatic nerves of adult female Sprague-Dawley rats (n = 20) were injected with a demyelinating agent immediately after transection injury. The sciatic nerves were harvested 1 month (n = 5) and 2 months (n = 5) after surgery. In the control groups, the cut nerves were reapproximated without demyelination therapy. The lesion containing length of nerve was cut into 1-mm transverse blocks and processed to preserve orientation. Specimens were evaluated using structural and immunohistochemical analyses.
A single epineural injection of complement proteins plus antibodies to galactocerebroside resulted in demyelination followed by Schwann cell remyelination. At 1 month, remyelination was clearly shown throughout the injured sciatic nerve segment. At 2 months, there was a statistically significant increase in peripheral nerve regeneration following demyelination therapy as evidenced by total axon count, axon density, and fiber diameter.
This study demonstrates enhanced histomorphologic nerve regeneration in the rat sciatic nerve after local delivery of experimental, immunologic demyelination following transection injury. It highlights the utility of demyelination in peripheral nerve regeneration. This therapy may be applicable for tissue-engineered constructs, cell-based systems, and nerve transfers to improve outcomes in peripheral nervous system injuries.
我们最近的实验表明,脱髓鞘可增强成年大鼠坐骨神经挫伤后的周围神经再生。脱髓鞘在坐骨神经横断模型的周围神经再生中的作用尚未阐明。我们假设:(1)实验性免疫脱髓鞘后,损伤区域内的轴突再生增加;(2)再生轴突部分源自近端运动轴突。
成年雌性Sprague-Dawley大鼠(n = 20)的坐骨神经在横断损伤后立即注射脱髓鞘剂。术后1个月(n = 5)和2个月(n = 5)收获坐骨神经。在对照组中,切断的神经在未进行脱髓鞘治疗的情况下重新对接。将含有神经的损伤段切成1毫米的横向块,并进行处理以保持方向。使用结构和免疫组织化学分析对标本进行评估。
单次神经外膜注射补体蛋白加半乳糖脑苷脂抗体导致脱髓鞘,随后雪旺细胞重新髓鞘化。在1个月时,整个损伤的坐骨神经段均明显显示出重新髓鞘化。在2个月时,脱髓鞘治疗后周围神经再生有统计学上的显著增加,总轴突计数、轴突密度和纤维直径证明了这一点。
本研究表明,在横断损伤后局部进行实验性免疫脱髓鞘后,大鼠坐骨神经的组织形态学神经再生增强。它突出了脱髓鞘在周围神经再生中的效用。这种疗法可能适用于组织工程构建体、基于细胞的系统和神经移植,以改善周围神经系统损伤的结果。