BETA(编程语言)
分泌物
磷酸化
卡帕
神经母细胞瘤
淀粉样蛋白(真菌学)
块(置换群论)
化学
细胞生物学
生物
生物化学
细胞培养
遗传学
哲学
语言学
计算机科学
无机化学
程序设计语言
数学
几何学
作者
Nihar R. Pandey,Karim R. Sultan,Erin Twomey,Daniel L. Sparks
出处
期刊:Neuroscience
[Elsevier]
日期:2009-12-01
卷期号:164 (4): 1744-1753
被引量:22
标识
DOI:10.1016/j.neuroscience.2009.09.062
摘要
Inflammation and oxidative stress have been shown to play a critical role in the pathophysiology that leads to neurodegeneration. Omega-6 phospholipids, e.g. dilinoleoylphosphatidylcholine (DLPC), have been shown to have anti-inflammatory properties and therefore experiments were undertaken to determine whether DLPC can prevent inflammatory neurodegenerative events in the model neuronal cell line, SH-SY5Y. Tumor necrosis factor (TNF-α) and H2O2 activate mitogen-activated protein kinase (MAPK) in SH-SY5Y cells within 5 min and this activation is completely blocked by DLPC (12 μM). DLPC blocks IκBα phosphorylation in the SH-SY5Y cells and prevents the phosphorylation and activation of nuclear factor-kappa B (NF-κB). The phospholipid inhibits induction of MAPK and NF-κB in similar fashion to the MEK1/2-inhibitor, U0126 (10 μM). DLPC completely abolishes TNF-α, H2O2 and lipopolysaccaride (LPS)-induced neuronal tau phosphorylation. Cellular amyloid precursor protein levels are reduced by DLPC and LPS-induced amyloid-β expression and secretion in SH-SY5Y cells are completely blocked by DLPC. Taken together, these data suggest that DLPC can act through MAPK to block neuronal inflammatory cascades and prevent potential pathological consequences in the neuronal metabolism of amyloid and tau proteins.
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