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以亚急性CO中毒小鼠脑组织Ca2 + -Mg2 + ATPase、SOD、MAO -B活性 ,LPO含量以及血皮质醇浓度的变化为观察指标 ,进行亚急性一氧化碳 (CO)中毒致小鼠迟发性学习记忆障碍的机制研究。结果显示 ,亚急性CO中毒小鼠脑组织SOD、Ca2 + -Mg2 + ATPase活性、LPO含量以及血皮质醇浓度均无显著改变 ;而MAO -B活性明显增加 ,地塞米松对皮质醇分泌的抑制率大为下降。提示 ,亚急性CO中毒所致小鼠迟发性学习记忆障碍可能涉及单胺能神经及其递质的改变 ,以及与下丘脑 -垂体 -肾上腺皮质轴功能调节失控有关 ;而与脂质过氧化 ,Ca2 + 平衡关系不大。
To subacute CO poisoning mice brain Ca2 + -Mg2 ATPase, SOD, MAO-B activity, LPO content and blood cortisol concentration changes were observed indicators of subacute carbon monoxide (CO) poisoning in mice induced by delayed Study on the Mechanism of Learning and Memory Disorders. The results showed that in the subacute CO poisoning mice brain SOD, Ca2 + -Mg2 + ATPase activity, LPO content and blood cortisol concentrations were not significantly changed; MAO-B activity was significantly increased dexamethasone cortisol secretion inhibition The rate of decline. Prompted that subacute CO poisoning induced delayed learning and memory impairment in mice may involve changes in monoamine nerves and their neurotransmitters, as well as with the hypothalamus-pituitary-adrenal axis dysregulation of regulation; and lipid peroxidation , Ca2 + balance has little to do.