發(fā)布時間：2018-04-22 21:28

  本文選題：小膠質(zhì)細(xì)胞 + 吞噬��； 參考：《廈門大學(xué)》2014年碩士論文

【摘要】：阿爾茨海默癥是一種主要的導(dǎo)致癡呆的老年疾病,其臨床特征為細(xì)胞外的淀粉樣沉淀和胞內(nèi)的神經(jīng)元纏結(jié)。淀粉樣沉淀的主要組成成分是淀粉樣蛋白(β-amyloid, Aβ)。大腦內(nèi)的Aβ的產(chǎn)生和降解的平衡被擾亂是現(xiàn)在比較公認(rèn)的阿爾茨海默癥的發(fā)病機制。Aβ分為可溶性和不可溶性兩種形式,研究顯示可溶性的Ap比不可溶的Aβ的毒性更大,Ap的清除速度即使有很緩慢的降低也會導(dǎo)致Aβ的聚集,進(jìn)而產(chǎn)生Aβ的沉積。小膠質(zhì)細(xì)胞是中樞神經(jīng)系統(tǒng)中的一種巨噬細(xì)胞,之前的研究顯示小膠質(zhì)細(xì)胞可以通過液相的大胞飲途徑,在Ap的內(nèi)吞和降解中發(fā)揮重要的作用,但其具體機制還不是很清楚。在本研究中我們發(fā)現(xiàn)與N2a神經(jīng)膠質(zhì)瘤細(xì)胞相比,BV-2小膠質(zhì)細(xì)胞具有很強的內(nèi)吞Ap的能力,不僅能較快速并且能內(nèi)吞更多的Ap；我們接著發(fā)現(xiàn)小膠質(zhì)細(xì)胞有多重內(nèi)吞Ap的方式；隨著Aβ被吞進(jìn)小膠質(zhì)細(xì)胞后,能很快到達(dá)溶酶體進(jìn)而被降解；我們通過ELISA方法量化兩種細(xì)胞降解Ap的能力,發(fā)現(xiàn)小膠質(zhì)細(xì)胞能降解更多的Ap。我們的研究還發(fā)現(xiàn)Ap在小膠質(zhì)細(xì)胞中的轉(zhuǎn)運有兩條途徑：再循環(huán)途徑和降解途徑,而且在小膠質(zhì)細(xì)胞中Aβ主要是經(jīng)降解途徑降解,都說明小膠質(zhì)細(xì)胞有很強的降解Aβ的能力。 我們的研究揭示了小膠質(zhì)細(xì)胞在淀粉樣蛋白的降解中發(fā)揮的作用,表明了小膠質(zhì)細(xì)胞在阿爾茨海默癥的病程發(fā)展中有重要的作用,這些研究為深入揭示阿爾茨海默癥的發(fā)病機制提供了新的信息。
[Abstract]:Alzheimer's disease is a major senile disease leading to dementia, its clinical characteristics are extracellular amyloid precipitation and intracellular neuronal tangles. The main component of amyloid precipitation is amyloid (A 尾 -amyloid). The disruption of the balance between the production and degradation of A 尾 in the brain is now more commonly recognized as the pathogenesis of Alzheimer's disease. A 尾 is divided into soluble and insoluble forms. The results show that soluble Ap is more toxic than insoluble A 尾. The scavenging rate of Ap can lead to the accumulation of A 尾 and the deposition of A 尾, even if it decreases slowly. Microglia are a kind of macrophages in the central nervous system. Previous studies have shown that microglia can play an important role in the endocytosis and degradation of AP through the liquid phase macrocytic pathway, but its specific mechanism is not very clear. In this study, we found that BV-2 microglia cells had a strong ability to endocytosis of AP, not only faster but also more Apps than N2a glioma cells, and then we found the way of multiple endocytosis of Ap in microglia cells. When A 尾 was swallowed into microglia, the lysosome was quickly reached and then degraded. We quantified the ability of two kinds of cells to degrade AP by ELISA method, and found that microglia could degrade more App. We also found that there are two pathways for the transport of AP in microglia: recirculation pathway and degradation pathway, and A 尾 in microglia is mainly degraded by degradation pathway, indicating that microglia have a strong ability to degrade A 尾. Our study revealed the role of microglia in amyloid degradation, suggesting that microglia play an important role in the progression of Alzheimer's disease. These studies provide new insights into the pathogenesis of Alzheimer's disease.
【學(xué)位授予單位】：廈門大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2014
【分類號】：R749.16

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