Longo F M, Powell H C, Lebeau J, Gerrero M R, Heckman H, Myers R R
Muscle Nerve. 1986 Jun;9(5):385-93. doi: 10.1002/mus.880090502.
Nerve regeneration across a 10-mm gap was delayed in streptozotocin diabetic rats 3 and 4 weeks after transecting the sciatic nerve. Opposite ends of each cut nerve were introduced into a silicone tube, leaving a 10-mm gap. Electron microscopy was used to evaluate the progress of regeneration in sections at 2-mm intervals across the 10-mm gap. After 3 weeks, control axons had bridged the 10-mm gap, and myelin sheaths extended for 6-8 mm. By contrast, axons and their myelin sheaths were seen no further than 2 mm from the proximal stump in diabetic animals. By 4 weeks, axons had bridged the gap in diabetics; however, they appeared immature and showed dystrophic changes. The findings suggest that although regeneration does occur in diabetic nerves, it is significantly delayed and qualitatively impaired.
在切断坐骨神经3周和4周后，链脲佐菌素诱导的糖尿病大鼠的神经再生跨越10毫米间隙的过程出现延迟。将每条切断神经的相对两端插入硅胶管中，留出10毫米的间隙。利用电子显微镜在跨越10毫米间隙的每隔2毫米处的切片中评估再生进程。3周后，对照轴突已跨越10毫米间隙，髓鞘延伸了6 - 8毫米。相比之下，在糖尿病动物中，轴突及其髓鞘距近端残端不超过2毫米。到4周时，轴突已在糖尿病动物中跨越间隙；然而，它们看起来不成熟并表现出营养不良性改变。这些发现表明，尽管糖尿病神经中确实会发生再生，但再生明显延迟且在质量上受损。
