叠氮钠造成脑线粒体损伤模型的研究现状

Investigations of cerebral mitochondrial impairment model induced by sodium azide

现已证明 ,线粒体缺陷与阿尔茨海默病 (AD)的发生密切相关 ,其中AD患者细胞色素C氧化酶 (COX)活性的降低明显且特异。叠氮钠 (NaN3 ) ,一种特异性COX抑制剂 ,可以损伤线粒体活性 ,建立具有部分类似AD病理改变的动物和细胞模型。它可以导致动物学习记忆功能障碍 ,其可能的机制包括细胞骨架结构破坏 ,Aβ沉积 ,氧化损伤 ,离子内稳态破坏 ,细胞膜损伤以及神经递质异常。NaN3 造成的脑线粒体损伤模型为AD机理和治疗药物的研究提供了新的途径。

It is proved that the mitochondrial defects relat ive closely to Alzheimer disease(AD), the activity of cytochrome C oxidase(C OX ) reduces obviously and specifically in AD patients. Investigators use sodium az ide(NaN 3), a selective inhibitor of COX, to impair the mitochondrial activity and establish the animal and cell models which have pathological changes similar to AD. NaN 3 can induce decline of learning and memory activity in animal. The mechanisms may include the impairment of neurocyte framework, β-amyloid pro tein deposition, oxidative damage, breaking of intracellular ionic steady state, impairment of cell membrane and abnormality of neurotransmitter. The cerebral m itochondrial impairment model provides a new method to investigate the pathologi es and medicines of AD.