一氧化氮与帕金森病大鼠模型神经损伤的研究  

Studies on nitric oxide and neuronal damage in rat model of Parkinson's disease

作　　者：周国庆 周孝达[2] 金泳清 陈光辉 王桂松 

机构地区：[1]南京军区南京总院神经内科,江苏南京210002 [2]上海第二医科大学仁济医院神经内科,上海200023

出　　处：《中风与神经疾病杂志》2000年第5期288-289,共2页Journal of Apoplexy and Nervous Diseases

摘　　要：目的　研究一氧化氮 (NO)在帕金森病 (PD)大鼠模型神经损伤中的作用。方法　用高效液相色谱电化学法 (HPL C- ET)及还原型辅酶 (NADPH)黄递酶组化法观察 NO在 PD大鼠模型神经损伤中的作用。结果　神经型一氧化氮合成酶 (n NOS)抑制剂 7-硝基吲唑 (7- NI)明显减少 6 -羟基多巴胺 (6 - OHDA )引起的纹状体多巴胺及其代谢产物的降低 (P<0 .0 1) ;纹状体 NADPH黄递酶阳性神经元可抵抗 6 - OHDA的损伤。结论　来源于神经元的 NO参与了 PD大鼠模型的神经损伤过程。Objective To investigate the role of nitric oxide (NO) in neuronal damage in the rat model of Parkinson ,s disease (PD). Methods The role of nitric oxide (NO) in 6 hydroxydopamine(6 OHDA) treated rat model of PD was investigated by using HPLC ET and NADPH diaphorase histochemistry. Results 7 nitroindazole (7 NI),a selective inhibitor of neuronal nitric oxide synthase (nNOS) may significantly decrease 6 OHDA induced deplection of striatal dopamine and its metabolite,and the NADPH diaphorase containing neuron in striatum could resist the 6 OHDA neurotoxicity. Conclusions Neuronally derived NO participate in the neurotoxic mechanism of the rat model of PD

关 键 词：一氧化氮 帕金森病 6-羟基多巴胺 动物模型 

分 类 号：R742.502[医药卫生—神经病学与精神病学]