【摘要】：內(nèi)源甲醛代謝失調(diào)被認(rèn)為是導(dǎo)致阿爾茨海默病的危險(xiǎn)因素之一,甲醛蓄積會(huì)引起神經(jīng)細(xì)胞的死亡和認(rèn)知功能的降低.研究表明,細(xì)胞內(nèi)甲醛分布于溶酶體內(nèi),而溶酶體功能異常與神經(jīng)退行性疾病密切相關(guān).本文采用甲醛特異熒光探針,在氧化應(yīng)激條件下,檢測(cè)到小鼠腦微血管內(nèi)皮細(xì)胞株bEnd.3和小鼠神經(jīng)瘤母細(xì)胞株N2a溶酶體內(nèi)甲醛明顯升高;在慢性腦低灌注大鼠動(dòng)物模型中,其腦神經(jīng)細(xì)胞的溶酶體內(nèi)甲醛也升高(P0.01);LeuLeuOMe處理bEnd.3細(xì)胞,使其溶酶體膜通透性增加,導(dǎo)致細(xì)胞內(nèi)甲醛蓄積,而胞外甲醛降低.以上結(jié)果證明,溶酶體具有儲(chǔ)存和轉(zhuǎn)運(yùn)甲醛的功能,如果溶酶體出現(xiàn)結(jié)構(gòu)與功能的異常,會(huì)導(dǎo)致甲醛代謝失調(diào),造成認(rèn)知損害.
[Abstract]:Endogenous formaldehyde metabolism disorder is considered to be one of the risk factors leading to Alzheimer's disease. Formaldehyde accumulation can lead to the death of nerve cells and the decrease of cognitive function. The results showed that formaldehyde in cells was located in lysosomes, and abnormal lysosomal function was closely related to neurodegenerative diseases. Under oxidative stress, formaldehyde in lysosome of mouse brain microvascular endothelial cell line bEnd.3 and mouse neuroblastoma cell line N2a was detected by formaldehyde specific fluorescence probe. The level of formaldehyde in lysosome of brain nerve cells was also increased (P0.01); LeuLeuOMe treatment increased the permeability of lysosomal membrane of bEnd.3 cells, resulting in the accumulation of formaldehyde in cells and the decrease of extracellular formaldehyde. These results suggest that lysosomes can store and transport formaldehyde. If the lysosome has abnormal structure and function, it will lead to maladjustment of formaldehyde metabolism and cognitive impairment.
【作者單位】： 中國(guó)科學(xué)院生物物理研究所腦與認(rèn)知科學(xué)國(guó)家重點(diǎn)實(shí)驗(yàn)室;中國(guó)科學(xué)院大學(xué);
【基金】：國(guó)家重點(diǎn)基礎(chǔ)研究發(fā)展計(jì)劃(973)資助項(xiàng)目(2012CB911004)~~
【分類號(hào)】：R749.16

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