Love A, Cotter M A, Cameron N E
Department of Biomedical Sciences, University of Aberdeen, UK.
Eur J Clin Invest. 1996 Aug;26(8):698-706. doi: 10.1111/j.1365-2362.1996.tb02156.x.
Peripheral nerve conduction velocity deficits in diabetic rats depend on decreased nerve perfusion, which may be related to increased free radical activity and impaired endogenous protection by the glutathione redox cycle. We studied the effect of treatment with the glutathione precursor N-acetyl-L-cysteine on nerve conduction, blood flow, maturation and regeneration. Two months of diabetes in mature rats caused 20% and 48% deficits in sciatic motor conduction velocity and endoneurial blood flow, respectively, which were largely corrected by N-acetyl-L-cysteine treatment during the second month. In young nondiabetic rats, sciatic motor conduction velocity increased by 31% over 6 weeks. Diabetes halved the conduction velocity maturation rate, however N-acetyl-L-cysteine treatment allowed a normal pattern of development. After 1 month of treated or untreated diabetes, the sciatic nerve was lesioned by a liquid nitrogen-cooled probe. Myelinated fibre regeneration distance, determined electrophysiologically, was reduced by 12.2% with diabetes; this was prevented by N-acetyl-L-cysteine treatment. Thus, the data stress the importance of free radical-mediated changes in the aetiology of experimental diabetic neuropathy.
糖尿病大鼠的周围神经传导速度缺陷取决于神经灌注减少，这可能与自由基活性增加以及谷胱甘肽氧化还原循环的内源性保护受损有关。我们研究了用谷胱甘肽前体N-乙酰-L-半胱氨酸治疗对神经传导、血流、成熟和再生的影响。成熟大鼠患糖尿病两个月后，坐骨神经运动传导速度和神经内膜血流分别出现了20%和48%的缺陷，在第二个月用N-乙酰-L-半胱氨酸治疗后，这些缺陷得到了很大程度的纠正。在年轻的非糖尿病大鼠中，坐骨神经运动传导速度在6周内提高了31%。然而，糖尿病使传导速度成熟率减半，不过N-乙酰-L-半胱氨酸治疗使发育模式恢复正常。在糖尿病治疗或未治疗1个月后，用液氮冷却的探针损伤坐骨神经。通过电生理学方法测定，糖尿病使有髓纤维再生距离减少了12.2%；而N-乙酰-L-半胱氨酸治疗可预防这种情况。因此，这些数据强调了自由基介导的变化在实验性糖尿病神经病变病因学中的重要性。
