Minocycline does not affect amyloid β phagocytosis by human microglial cells
Minocycline does not affect amyloid β phagocytosis by human microglial cells
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DOI：
10.1016/j.neulet.2007.01.052
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发表时间：
2007-04-06
影响因子：
2.5
通讯作者：
Veerhuis, Robert
中科院分区：
文献类型：
--
作者：
Familian, Atoosa;Eikelenboom, Piet;Veerhuis, Robert
在阿尔茨海默病（AD）脑中，活化的小胶质细胞聚集在含有淀粉样蛋白相关因子SAP和C1 q的淀粉样蛋白3（A β）斑块中。小胶质细胞通过促进A β斑块形成和促炎细胞因子的产生参与AD发病机制。另一方面，活化的小胶质细胞对A β的吞噬作用可以防止A β介导的神经毒性和A β斑块形成。米诺环素是一种四环素衍生物，在各种神经退行性疾病模型以及人类慢性神经系统疾病中具有神经保护作用。米诺环素减弱暴露于A β、SAP和C1 q混合物后人小胶质细胞TNF-α的释放在这里，我们证明了米诺环素下调人类小胶质细胞的促炎细胞因子的产生，而不影响其有益的活性，淀粉样蛋白β纤维的吞噬作用。(c)2007爱思唯尔爱尔兰有限公司保留所有权利。
Activated microglia accumulate in amyloid 3 (A beta) plaques containing amyloid associated factors SAP and C1q in Alzheimer's disease (AD) brain. Microglia are involved in AD pathogenesis by promoting A beta plaque formation and production of pro-inflammatory cytokines. On the other hand, phagocytosis of A beta by activated microglia may prevent A beta-mediated neurotoxicity and A beta plaque formation. Minocycline, a tetracycline derivative, is neuroprotective in various neurodegenerative models as well as human chronic neurological disorders. Minocycline attenuates the release of TNF-alpha by human microglia upon exposure to a mixture of A beta, SAP and C1q. Here, we demonstrate that minocycline down-regulates the production of pro-inflammatory cytokines by human microglia without affecting their beneficial activity, phagocytosis of amyloid beta fibrils. (c) 2007 Elsevier Ireland Ltd. All rights reserved.