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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。
In this paper, gerbils were used to make animal models of delayed neuronal damage. From the point of view of free radical metabolism, we observed the changes of five biochemical indexes of 6 zones in 6 zones of animal brain before and after ischemia. The results showed that the hippocampal CA 1 region has its own unique variation, highlighting the following: 1 to 96 hours after short-term cerebral ischemia in the reperfusion process, the content of free radicals showed a sustained increase in mitochondrial manganese superoxide Dismutase decreased progressively and the changes of copper-zinc superoxide dismutase and lipid peroxide content were both volatile. These changes were absent in the rest of the brain except for the CA_2 region. The experimental results show that: free radical metabolism disorders are the key to the pathogenesis of delayed neuronal injury. Further study found that Aniacetam, tofu glycosides and nicardipine on these free radical metabolism disorders have varying degrees of improvement.