Cameron N E, Leonard M B, Ross I S, Whiting P H
Diabetologia. 1986 Mar;29(3):168-74. doi: 10.1007/BF02427088.
This study examined the effects of an aldose reductase inhibitor, Sorbinil, on neuropathy over a 6-month period in streptozotocin-diabetic rats. Sorbinil treatment prevented the 10-fold increase in nerve sorbitol found with diabetes. It produced a 60% improvement in tibial nerve motor conduction velocity after 6 months. Morphometric profiles of nerves were also normalized. Axon area was reduced by 14% in untreated diabetic rats compared to age-matched controls, whereas Sorbinil-treated animals showed normal age-related axon growth. Myelin area was increased by 28% in untreated diabetic animals, but was the same as age-matched controls with Sorbinil treatment. Nerve myo-inositol levels were reduced by 45% after three months of untreated diabetes, but were normal after six months. Sorbinil treatment tended to restore myo-inositol levels toward normal over the shorter time period. It was concluded that axon growth retardation is the most likely cause of the conduction deficit seen in long-term experimental diabetes.
本研究在6个月期间内，考察了醛糖还原酶抑制剂索比尼尔对链脲佐菌素诱导的糖尿病大鼠神经病变的影响。索比尼尔治疗可防止糖尿病大鼠神经山梨醇含量增加10倍。6个月后，它使胫神经运动传导速度提高了60%。神经的形态学特征也恢复正常。与年龄匹配的对照组相比，未治疗的糖尿病大鼠轴突面积减少了14%，而接受索比尼尔治疗的动物显示出与年龄相关的正常轴突生长。未治疗的糖尿病动物髓鞘面积增加了28%，但接受索比尼尔治疗的动物与年龄匹配的对照组相同。未经治疗的糖尿病3个月后神经肌醇水平降低了45%，但6个月后恢复正常。索比尼尔治疗倾向于在较短时间内使肌醇水平恢复正常。研究得出结论，轴突生长迟缓是长期实验性糖尿病中传导缺陷最可能的原因。
