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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Promotion of β-amyloid production by C-reactive protein and its implications in the early pathogenesis of Alzheimer's disease
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Promotion of β-amyloid production by C-reactive protein and its implications in the early pathogenesis of Alzheimer's disease

机译：C反应蛋白促进β淀粉样蛋白产生及其对阿尔茨海默氏病早期发病的影响

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摘要

C-reactive protein (CRP) and β-amyloid protein (Aβ) are involved in the development of Alzheimer's disease (AD). However, the relationship between CRP and Aβ production is unclear. In vitro and in vivo experiments were performed to investigate the association of CRP with Aβ production. Using the rat adrenal pheochromocytoma cell line (PC12 cells) to mimic neurons, cytotoxicity was evaluated by cell viability and supernatant lactate dehydrogenase (LDH) activity. The levels of amyloid precursor protein (APP), beta-site APP cleaving enzyme (BACE-1), and presenilins (PS-1 and PS-2) were investigated using real-time polymerase chain reaction and Western blotting analysis. Aβ1-42 was measured by enzyme-linked immunosorbent assay. The relevance of CRP and Aβ as well as potential mechanisms were studied using APP/PS1 transgenic (Tg) mice. Treatment with 0.5-4.0 μM CRP for 48 h decreased cell viability and increased LDH leakage in PC12 cells. Incubation with CRP at a sub-toxic concentration of 0.2 μM increased the mRNA levels of APP, BACE-1, PS-1, and PS-2, as well as Aβ1-42 production. CRP inhibitor reversed the CRP-induced upregulations of the mRNA levels of APP, BACE-1, PS-1, and PS-2, and the protein levels of APP, BACE-1, PS-1, and Aβ1-42, but did not reversed Aβ1-42 cytotoxicity. The cerebral levels of CRP and Aβ1-42 in APP/PS1 Tg mice were positively correlated, accompanied with the elevated mRNA expressions of serum amyloid P component (SAP), complement component 1q (C1q), and tumor necrosis factor-α (TNF-α). These results suggest that CRP cytotoxicity is associated with Aβ formation and Aβ-related markers expressions; CRP and Aβ were relevant in early-stage AD; CRP may be an important trigger in AD pathogenesis.
机译：C反应蛋白（CRP）和β淀粉样蛋白（Aβ）参与了阿尔茨海默氏病（AD）的发展。但是，CRP和Aβ产生之间的关系尚不清楚。进行体外和体内实验以研究CRP与Aβ产生的关系。使用大鼠肾上腺嗜铬细胞瘤细胞系（PC12细胞）模仿神经元，通过细胞活力和上清液乳酸脱氢酶（LDH）活性评估细胞毒性。使用实时聚合酶链反应和蛋白质印迹分析研究了淀粉样蛋白前体蛋白（APP），β位APP裂解酶（BACE-1）和早老素（PS-1和PS-2）的水平。通过酶联免疫吸附测定法测定Aβ1-42。使用APP / PS1转基因（Tg）小鼠研究了CRP和Aβ的相关性以及潜在的机制。用0.5-4.0μMCRP处理48小时会降低细胞活力，并增加PC12细胞中LDH的泄漏。以0.2μM的亚毒性浓度与CRP一起孵育可提高APP，BACE-1，PS-1和PS-2的mRNA水平以及Aβ1-42的产生。 CRP抑制剂逆转了CRP诱导的APP，BACE-1，PS-1和PS-2 mRNA水平以及APP，BACE-1，PS-1和Aβ1-42蛋白水平的上调，但确实如此不逆转Aβ1-42细胞毒性。 APP / PS1 Tg小鼠的脑CRP和Aβ1-42水平呈正相关，并伴有血清淀粉样P成分（SAP），补体成分1q（C1q）和肿瘤坏死因子-α（TNF-α）mRNA表达的升高。 α）。这些结果表明，CRP的细胞毒性与Aβ的形成和Aβ相关标志物的表达有关。 CRP和Aβ与早期AD有关。 CRP可能是AD发病机制中的重要触发因素。

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