【摘要】 目的:探讨一氧化氮(NO)与超氧化物歧化酶(SOD)对迟发性神经元坏死(DND)发生、发展的影响及两者的关系。方法:Wistar大鼠制做血管阻断(four-vessel occlusion,4VO)模型,给予小剂量一氧化氮合酶(NOS)抑制剂干预,通过分光光度法测定不同脑区中NO和SOD的含量。结果:实验组再灌流期一氧化氮代谢产物(NO x)(NO2+NO3)含量与对照组比较升高不明显(P>0．05),随再灌流时间的延长逐渐递减并低于对照组(P<0．05或0．01),SOD在海马区再灌流期明显下降(P<0．05或0．01),而NOS抑制剂对其无明显影响。相关性分析显示,脑组织中NO x与SOD含量呈正相关关系(r=0．9624,P<0．05或0．01)。结论:小剂量NOS抑制剂在DND中具有保护神经细胞受损伤作用,SOD不仅能够消除超氧阴离子,而且对 NO x自由基也有较强的消除作用。更多还原

【Abstract】 Objective To study the influences of nitric oxide (NO) and superoxide dismutase (SOD) in genesis and progress of delayed neuronal death (DND) in rats. Methods Wistar rats were used to establish the models of four-vessel occlusion (4VO) and were treated with small dose of nitric oxide synthase (NOS) inhibitor [N-nitro-L-arginine (NNLA)]. The levels of NO and SOD in the brain tissues of the models were determined by spectrophotometry. Results The level of NO x (NO2 + NO3 ) in the experiment group was not significantly increased compared with control group (P>0. 05). When reperfusion time was prolonged, the level of NO in the experiment group was decreased gradually and was lower than that in control group (P<0. 05 or 0. 01). The level of SOD in hippocampus region was decreased distinctly (P<0. 05 or 0. 01) and was not influenced by NNLA. The relativity analysis showed that the levels of NO and SOD in brain tissues were highly relative (r=0. 9624, P<0. 05 or 0. 01). Conclusion Small dose of NOS inhibitor has the effect to protect neuron in DND rats. SOD can not only clean out superoxide negativeion, but also eliminate reactive oxygen species of NO x.更多还原