Ekström A R, Tomlinson D R
Department of Zoophysiology, University of Lund, Sweden.
J Neurol Sci. 1989 Nov;93(2-3):231-7. doi: 10.1016/0022-510x(89)90193-7.
Rats with streptozotocin-induced diabetes have a decreased rate of sciatic nerve regeneration. We studied the effects on this defect of treatment with the aldose reductase inhibitor, ponalrestat (25 mg/kg per day via an endogastric tube). The nerves of diabetic rats were crush-injured at 5 weeks of diabetes and regeneration evaluated 7 days later with the pinch-reflex test. Ponalrestat treatment was started at day 3 after streptozotocin injection and was continued for the whole experimental period, i.e. until 6 weeks of diabetes. The treatment prevented effectively the accumulation of sorbitol and fructose in the nerves of diabetic rats, but was without effect on the sciatic nerve regeneration (controls 21.8 +/- 1.2 mm/7 days (mean +/- SEM, n = 6), untreated diabetics 15.8 +/- 1.8 (n = 7), ponalrestat-treated diabetics 16.2 +/- 1.0 (n = 10]. The results indicate that there is no connection between increased sorbitol pathway flux and impaired regeneration in streptozotocin diabetic rats.
链脲佐菌素诱导的糖尿病大鼠坐骨神经再生速率降低。我们研究了醛糖还原酶抑制剂泊那司他（通过胃内管给药，每天25毫克/千克）对这种缺陷的治疗效果。糖尿病大鼠的神经在糖尿病5周时受到挤压损伤，并在7天后通过捏反射试验评估再生情况。泊那司他治疗在链脲佐菌素注射后第3天开始，并持续整个实验期，即直到糖尿病6周。该治疗有效地阻止了糖尿病大鼠神经中山梨醇和果糖的积累，但对坐骨神经再生没有影响（对照组21.8±1.2毫米/7天（平均值±标准误，n = 6），未治疗的糖尿病大鼠15.8±1.8（n = 7），泊那司他治疗的糖尿病大鼠16.2±1.0（n = 10）。结果表明，在链脲佐菌素糖尿病大鼠中，山梨醇途径通量增加与再生受损之间没有关联。
