迟发性神经元损伤发生中与自由基的作用机制及防治

本文用沙土鼠制作迟发性神经元损伤动物模型。从自由基代谢角度观察了动物脑6个分区5种生化指标在缺血前后7个时相的变化情况。结果表明,海马CA_1区有其独特变化规律,突出地表现为:在短时脑缺血后1—96小时的重灌流过程中,自由基含量呈持续性升高,线粒体中的锰超氧化物歧化酶则呈进行性降低,铜锌超氧化物歧化酶和脂质过氧化物含量的变化则都具有波动性。在除CA_2区外的其余部分脑组织中则没有上述这些变化。本实验的结果表明:自由基代谢紊乱是迟发性神元经损伤发生机理中的关键环节。经进一步研究发现,Aniacetam、豆腐果甙和尼卡地平对这种自由基代谢紊乱都有不同程度的改善作用。

Free radicals in delayed neuronal damage and prevention

In the present study, Mongolian gerbil was used to make delayed neuronal damage (IND) animal model. In 6 different brain regions, 5 kinds of biochemical indexes in the aspect of free radical metabolism were measured at 7 time phases during ischemia and reperfusion. The results showed that, after transient cerebral ischemia and during reperfusion, some unique changes appeared tn hippocampal CA1 sector, which were characterized by the persistent increase of free radical content and persistent decrease of the Mn-SOD activity. The fluctuating changes could be seen in Cu, Zn-SOD activity and lipid peroxide content. There were no significant changes in the brain regions other than CA1 sector. It is concluded that the disturbance of free radical metabolism play a key role in the occur. fence of DND. It was also observed that Aniracetam, Helicid and Nieardipine had some control effects to a certatn extent on the free radical disturbance above in hippocampal CA1 sector of DND animals.