南方医科大学学报 ›› 2014, Vol. 34 ›› Issue (08): 1158-.

• • 上一篇    下一篇

糖尿病大鼠神经病理疼痛增强脊髓神经型一氧化氮合酶的表达

赵伟成,廖美娟,张文璇,王汉兵,刘洪珍,杨承祥,张斌   

  • 出版日期:2014-08-20 发布日期:2014-08-20

Change of spinal neuronal nitric oxide synthase expression in rats with painful diabetic
neuropathy

  • Online:2014-08-20 Published:2014-08-20

摘要: 目的观察糖尿病大鼠神经病理性疼痛形成时脊髓神经型一氧化氮合酶(nNOS)表达的变化。方法60只SD大鼠,随机
分为糖尿病神经病理性疼痛大鼠组(DM组)和空白对照组(C组),n=30。DM组大鼠采用腹腔注射链尿佐菌素(STZ,60 mg/kg)
诱导糖尿病神经病理性疼痛,C组则注射等剂量的溶剂。于注射STZ前、注射STZ后2、7、14、21、28 d(T1~6)取尾静脉血测定血
糖;于T1、T3~6时用von Frey丝测定50%缩足反应阈值(PWT)并测量大鼠体质量;分别于T1、T3~6时处死各组6只大鼠,采用免疫印
迹的方法检测大鼠脊髓nNOS的表达。结果与C组相比,DM组大鼠注射STZ后血糖显著增高(P<0.01),体质量逐渐下降(P<
0.05);DM组大鼠于T4~6时PWT明显低于C组(P<0.05);DM组大鼠脊髓的nNOS的表达于T4~6时明显较C组增强(P<0.05);DM
组大鼠脊髓nNOS的表达与其PWT呈明显的负相关(P<0.01)。结论糖尿病神经病理性疼痛大鼠脊髓nNOS表达增强,可能参
与其疼痛的形成。

Abstract: Objective To observe the change of neuronal nitric oxide synthase (nNOS) expression in the spinal cord of diabetic
rats with painful diabetic neuropathy. Methods Sixty SD rats were randomized equally into painful diabetic neuropathy group
(DM group) and control group. Painful diabetic neuropathy was induced by intraperitoneal injection with STZ (60 mg/kg) in
DM group, and the rats in the control group received a solvent injection. Blood glucose levels were measured before and at 2,
7, 14, 21, and 28 days after STZ injection (T1-6 respectively). Responses to the mechanical stimulus were measured with von Frey
filament, and 50% paw withdraw threshold (PWT) and body weight were recorded at T1 and T3-6. At T1 and T3-6, 6 rats from
each group were sacrificed to examine the expression of nNOS in the lumbar segments of the spinal cord using Western blotting.
Results The level of blood glucose increased while the body weight decreased significantly after STZ injection in DM
group (P<0.05). Comparing to those in the control group, PWT decreased while spinal nNOS expression increased significantly
in DM group at T4-6 (P<0.05) showing an inverse correlation between them (P<0.01). Conclusion The enhanced expression of
spinal nNOS might be involved in the pathogenesis of painful diabetic neuropathy in rats.