摘要
本研究的目的是探讨改变核转录因子的水平κBp65(NF-κBp65)、单核细胞化学引诱物蛋白1(MCP-1 / CCL-2)和巨噬细胞炎性蛋白- 1α(MIP-1α/ CCL-3)关系的表达α3烟碱乙酰胆碱受体(乙酰胆在阿尔茨海默病(AD)的发病机理。阿尔茨海默病和年龄的事后人脑控制个人,SH-SY5Y和U87MG细胞株暴露β-amyloid肽(Aβ),以及SH-SY5Y的细胞α3抑制了乙酰siRNA被用来研究可能的表达变化的目标如NF-κBp65 MCP-1,MIP-1αα3乙酰胆。免疫组织化学结果显示NF-κBp65免疫反应性的增加,MCP-1和MIP-1α神经元的大脑海马和颞叶和额叶区域的阿尔茨海默病。NF-κBp65水平,MCP-1 MIP-1α蛋白质和mRNA水平都显著上调SH-SY5Y和U87MG细胞暴露于Aβ1-42,虽然表明α3 Aβ1-42暴露SH-SY5Y细胞乙酰胆是衰减的。有趣的是,在SH-SY5Y细胞受到α3乙酰信使rna,NF-κBp65,MCP-1 MIP-1α升高。NF -κB和趋化因子的高表达可能参与表达减少α3乙酰胆在AD的发病机制。
关键词: 阿尔茨海默氏症、大脑、β-amyloid肽、NF-κBp65、MCP-1、MCP-1α、α3乙酰胆。
Current Alzheimer Research
Title:Elevations in the Levels of NF-κB and Inflammatory Chemotactic Factors in the Brains with Alzheimer’s Disease - One Mechanism May Involve α3 Nicotinic Acetylcholine Receptor
Volume: 13 Issue: 11
Author(s): Yuan Liao, Xiao-Lan Qi, Ying Cao, Wen-Feng Yu, Rivka Ravid, Bengt Winblad, Jin-Jing Pei, Zhi-Zhong Guan
Affiliation:
关键词: 阿尔茨海默氏症、大脑、β-amyloid肽、NF-κBp65、MCP-1、MCP-1α、α3乙酰胆。
摘要: The purpose of this study was to investigate the alterations in the levels of nuclear factor κBp65 (NF-κBp65), monocyte chemoattractant protein 1 (MCP-1/CCL-2) and macrophage inflammatory protein 1α (MIP-1α/CCL-3) in relationship to the expression of α3 nicotinic acetylcholine receptor (nAChR) during the pathogenesis of Alzheimer’s disease (AD). The post-mortem human brains of AD and age-matched control individuals, SH-SY5Y and U87MG cell lines exposed to β-amyloid peptide (Aβ), as well as the SH-SY5Y cells in which α3 nAChR was down-regulated by siRNA were used to study the possible expression changes of the targets such as NF-κBp65, MCP-1, MIP-1α and α3 nAChR. The immunohistochemistry results showed the increased immunoreactivities of NF-κBp65, MCP-1 and MIP-1α in neurons in hippocampal and temporal and frontal regions of AD brains. Levels of NF-κBp65, MCP-1 and MIP-1α at both protein and mRNA levels were all significantly up-regulated in SH-SY5Y and U87MG cells exposed to Aβ1-42, while expression of α3 nAChRs in Aβ1-42 exposed SH-SY5Y cells was attenuated. Interestingly, in the SH-SY5Y cells subjected to α3 nAChR mRNA silencing, expression of NF-κBp65, MCP-1 and MIP-1α was elevated. The elevated expressions of NF- κB and chemokines may be involved by decreased expression of α3 nAChRs during the pathogenesis of AD.
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Yuan Liao, Xiao-Lan Qi, Ying Cao, Wen-Feng Yu, Rivka Ravid, Bengt Winblad, Jin-Jing Pei, Zhi-Zhong Guan , Elevations in the Levels of NF-κB and Inflammatory Chemotactic Factors in the Brains with Alzheimer’s Disease - One Mechanism May Involve α3 Nicotinic Acetylcholine Receptor, Current Alzheimer Research 2016; 13 (11) . https://dx.doi.org/10.2174/1567205013666160703174254
DOI https://dx.doi.org/10.2174/1567205013666160703174254 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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