Calcutt N A, Tomlinson D R, Willars G B
Department of Physiology and Pharmacology, Medical School, Queen's Medical Centre, Nottingham, England.
J Neurochem. 1988 May;50(5):1478-83. doi: 10.1111/j.1471-4159.1988.tb03033.x.
This study measured axonal transport of 6-phosphofructokinase (PFK) and aldolase activities in the sciatic nerves of rats with short-term streptozotocin-induced diabetes. The diabetic rats showed deficits in anterograde (69% of controls; p less than 0.001) and retrograde (33% of controls; p less than 0.01) accumulations of PFK activity as well as its content per unit length of unconstricted sciatic nerve (86% of controls; p less than 0.05). There were no accumulation deficits in aldolase activity in the nerves of the diabetic rats, although the activity per unit length of unconstricted nerve was deficient (81% of controls; p less than 0.05). Treatment of diabetic rats with mixed bovine brain gangliosides (10 mg/kg of body weight/day, i.p.) did not affect the deficit in PFK activity in unconstricted nerve (84% of ganglioside-treated controls; p less than 0.01), but all the other defects in enzyme activities were prevented completely. The diabetic rats also showed a reduction of 7% (p less than 0.01) in sciatic nerve dry weight per unit length, which was prevented by ganglioside treatment. In contrast, the reduced motor nerve conduction velocity, accumulation of polyol pathway metabolites, and depletion of myo-inositol, characteristic of untreated short-term diabetes, were unaffected by ganglioside treatment.
本研究测量了短期链脲佐菌素诱导的糖尿病大鼠坐骨神经中6-磷酸果糖激酶（PFK）的轴突运输及醛缩酶活性。糖尿病大鼠在未受压迫的坐骨神经中，顺行性（为对照组的69%；p<0.001）和逆行性（为对照组的33%；p<0.01）PFK活性积累以及其单位长度含量（为对照组的86%；p<0.05）均出现缺陷。糖尿病大鼠神经中的醛缩酶活性虽未出现积累缺陷，但未受压迫神经的单位长度活性存在不足（为对照组的81%；p<0.05）。用混合牛脑神经节苷脂（10mg/kg体重/天，腹腔注射）治疗糖尿病大鼠，未受压迫神经中的PFK活性缺陷未受影响（为神经节苷脂治疗对照组的84%；p<0.01），但酶活性的所有其他缺陷均被完全预防。糖尿病大鼠未受压迫神经单位长度的坐骨神经干重也降低了7%（p<0.01），神经节苷脂治疗可预防此现象。相比之下，未治疗的短期糖尿病特有的运动神经传导速度降低、多元醇途径代谢产物积累和肌醇消耗，不受神经节苷脂治疗的影响。
