Sasaki T, Yasuda H, Maeda K, Kikkawa R
Third Department of Medicine, Shiga University of Medical Science, Otsu, Japan.
Neuroreport. 1998 Jan 26;9(2):243-7. doi: 10.1097/00001756-199801260-00013.
To evaluate the role of nitric oxide synthase (nNOS) in the pathogenesis of diabetic neuropathy, we investigated nociception and nNOS expression in dorsal root ganglion (DRG) of rats with streptozocin-induced diabetes. Paw withdrawal threshold to noxious mechanical stimuli was decreased in both L-NAME-treated and diabetic rats. The number of NADPH-diaphorase positive neurons was significantly decreased in untreated diabetic compared with control rats. Decreased expression of nNOS protein was confirmed by immunoblotting. Insulin treatment completely prevented decreases in withdrawal threshold and nNOS expression. Cyclic GMP content paralleled nNOS expression in experimental animals. These results suggest that decreased nNOS-cGMP system in DRG may play a role in the pathogenesis of diabetic sensory neuropathy.
为评估一氧化氮合酶（nNOS）在糖尿病性神经病变发病机制中的作用，我们研究了链脲佐菌素诱导的糖尿病大鼠背根神经节（DRG）中的伤害感受和nNOS表达。L-NAME处理组和糖尿病大鼠对有害机械刺激的爪部退缩阈值均降低。与对照大鼠相比，未经治疗的糖尿病大鼠中NADPH-黄递酶阳性神经元数量显著减少。免疫印迹证实nNOS蛋白表达降低。胰岛素治疗完全预防了退缩阈值和nNOS表达的降低。实验动物中环状GMP含量与nNOS表达平行。这些结果表明，DRG中nNOS-cGMP系统的降低可能在糖尿病性感觉神经病变的发病机制中起作用。
