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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Innate immunity and transcription of MGAT-Ⅲ and Toll-like receptors in Alzheimer's disease patients are improved by bisdemethoxycurcumin
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Innate immunity and transcription of MGAT-Ⅲ and Toll-like receptors in Alzheimer's disease patients are improved by bisdemethoxycurcumin

机译：双去甲氧基姜黄素可改善阿尔茨海默氏病患者的先天免疫力以及MGAT-Ⅲ和Toll样受体的转录

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摘要

We have tested a hypothesis that the natural product curcumi-noids, which has epidemiologic and experimental rationale for use in AD, may improve the innate immune system and increase amyloid-β (Aβ) clearance from the brain of patients with sporadic Alzheimer's disease (AD). Macrophages of a majority of AD patients do not transport Aβ into endosomes and lysosomes, and AD monocytes do not efficiently clear Aβ from the sections of AD brain, although they phagocytize bacteria. In contrast, macrophages of normal subjects transport Aβ to endosomes and lysosomes, and monocytes of these subjects clear Aβ in AD brain sections. Upon Aβ stimulation, mononuclear cells of normal subjects up-regulate the transcription of β-1,4-mannosyl-glycoprotein 4-β-N-acetylglucosaminyltransferase (MGAT3) (P < 0.001) and other genes, including Toll like receptors (TLRs), whereas mono-nuclear cells of AD patients generally down-regulate these genes. Defective phagocytosis of Aβ may be related to down-regulation of MGAT3, as suggested by inhibition of phagocytosis by using MGAT3 siRNA and correlation analysis. Transcription of TLR3. bditTLR4, TLRS, bditTLR7, TLR8, TLR9. and TLR10 upon Aβ stimulation is severely depressed in mononuclear cells of AD patients in comparison to those of control subjects. In mononuclear cells of some AD patients, the curcuminoid compound bisdemethoxycurcumin may enhance defective phagocytosis of Aβ, the transcription of MGAT3 and TLRs, and the translation of TLR2-4. Thus, bisdemethoxycurcumin may correct immune defects of AD patients and provide a previously uncharacterized approach to AD immunotherapy.
机译：我们已经测试了一种假设，即具有在AD中使用的流行病学和实验依据的天然产物姜黄素可能会改善散发性阿尔茨海默氏病（AD）患者大脑的先天免疫系统并增加淀粉样β（Aβ）清除率）。大多数AD患者的巨噬细胞不会将Aβ转运入内体和溶酶体，并且AD单核细胞尽管吞噬了细菌，但却无法有效清除AD脑切片中的Aβ。相反，正常受试者的巨噬细胞将Aβ转运至内体和溶酶体，这些受试者的单核细胞清除了AD脑切片中的Aβ。受到Aβ刺激后，正常个体的单核细胞上调β-1,4-甘露糖基糖蛋白4-β-N-乙酰氨基葡萄糖氨基转移酶（MGAT3）（P <0.001）和其他基因，包括Toll样受体（TLRs）的转录，而AD患者的单核细胞通常会下调这些基因。 Aβ的吞噬缺陷可能与MGAT3的下调有关，这是通过使用MGAT3 siRNA抑制吞噬作用和相关分析表明的。 TLR3的转录。 bditTLR4，TLRS，bditTLR7，TLR8，TLR9。与对照组相比，AD患者的单核细胞中Aβ和TLR10的刺激被严重抑制。在某些AD患者的单核细胞中，姜黄素类化合物双去甲氧基姜黄素可能会增强Aβ的吞噬缺陷，MGAT3和TLR的转录以及TLR2-4的翻译。因此，双去甲氧基姜黄素可以纠正AD患者的免疫缺陷，并提供AD免疫治疗以前未知的方法。

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