Aspirin-Triggered Lipoxin A4 Attenuates Lipopolysaccharide-Induced Intracellular ROS in BV2 Microglia Cells by Inhibiting the Function of NADPH Oxidase
Aspirin-Triggered Lipoxin A4 Attenuates Lipopolysaccharide-Induced Intracellular ROS in BV2 Microglia Cells by Inhibiting the Function of NADPH Oxidase
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DOI：
10.1007/s11064-012-0776-3
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发表时间：
2012-08-01
影响因子：
4.4
通讯作者：
Shang, You
中科院分区：
文献类型：
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作者：
Wu, Yan;Zhai, Heng;Shang, You
脂质已成为内源性抗炎症和解决关键事件的介质。然而，这些新型脂质介质对神经炎症的影响尚未被研究。小胶质细胞是感染和神经退行性疾病期间脑组织损伤的主要细胞。神经炎症条件共有的主要特征之一是NADPH氧化酶激活产生的活性氧（ROS）的增加。在这项研究中，我们研究了阿司匹林触发的脂素A(4) （ATL）是否调节BV2细胞中ROS的产生。用ATL预处理BV2细胞，以时间依赖性和浓度依赖性的方式阻断LPS触发的ROS生成。ATL抑制细胞质NADPH氧化酶亚基p47（phox）向细胞膜的易位以及NADPH氧化酶活性。综上所述，这些结果表明ATL抑制了BV2小胶质细胞中NADPH氧化酶介导的ROS生成，强烈表明ATL可能在对抗神经炎症的发生和进展中发挥重要作用。
Lipoxins have emerged as mediators of key events in endogenous anti-inflammation and resolution. However, the implication of these novel lipid mediators on neuroinflammation has not been investigated. Microglia is the major cells involved in brain tissue damage during infection and neurodegenerative diseases. One of the major features shared by neuroinflammation conditions is the increased production of reactive oxygen species (ROS) generated by NADPH oxidase activation. In this study, we have examined whether aspirin-triggered lipoxin A(4) (ATL) modulates ROS generation in BV2 cells. Pre-treatment of BV2 cells with ATL blocked ROS production triggered by LPS in the time-dependent and concentration-dependent manner. ATL inhibited the translocation of the cytoplasmic NADPH oxidase subunit p47(phox) to the cell membrane as well as NADPH oxidase activity. Taken together, these results demonstrate that ATL suppresses NADPH oxidase-mediated ROS generation in BV2 microglia cells, strongly indicating that ATL may play an important role against the development and progression of neuroinflammtion.