The Experiment of Edaravone on Primary Microglia Activation by Lipopolysaccharide

Qiao Ting Ting; Chen Zhong Yi; Dong Bao Lian; Yin Yan; Guo Ling

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Qiao Ting Ting , Chen Zhong Yi , Dong Bao Lian , Yin Yan , Guo Ling . The Experiment of Edaravone on Primary Microglia Activation by Lipopolysaccharide[J]. Journal of Kunming Medical University, 2018, 39(04): 5-10.

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Qiao Ting Ting , Chen Zhong Yi , Dong Bao Lian , Yin Yan , Guo Ling . The Experiment of Edaravone on Primary Microglia Activation by Lipopolysaccharide[J]. Journal of Kunming Medical University, 2018, 39(04): 5-10.

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The Experiment of Edaravone on Primary Microglia Activation by Lipopolysaccharide

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基金：国家自然科学基金资助项目 (81760228); 云南省教育厅科学研究基金资助项目 (2012Z093); 云南省科技厅科技计划青年基金资助项目 (2017FD193);

Received Date: 2018-01-11

Abstract

Abstract

Objective To explore the effect of Edaravone (EDA) on oxidative stress such as release of nitric oxide (NO) induced by Lipopolysaccharide (LPS) in activation of primary microglia. Me thods There were four groups including control, LPS, LPS + EDA and MAPK inhibitors + EDA + LPS in this study. The primary mixed glial cells were derived from the cortex of Sprague-Dawley rats which were 2 to 3-day old neonatal pups. The primary microglia were separated and purified by Biological Shaker after growing for about ten days. Griess Assay was used to detect NO secreted by activated microglia in four groups. Re s ults The shake-off microglial cells were confirmed as purity of 95% or up via fluorescence staining of CD68. Compared with the control group, NO product of microglial activation mediated by LPS significantly increased while NO value decreased in the group of EDA which was pretreatedt of EDA ahead of LPS for 24 hrs (P<0.05) . After addition of LPS, the incubation was remained for additional 24 h. In addition to EDA pretreatment for 24 h, the addition of three Mitogen-activated protein kinase inhibitors of MAPK signaling pathways were ahead of addition of EDA for 30 min, and then 10 ng/m Lof LPS was added to microglia. All of them incubated with the primary microglia for 24 h after the last addition. NO release was significantly reduced, the difference was statistically significant (P <0.05) .Conclus ion EDA treatment alone could inhibit the release of NO induced by LPS in primary microglia while EDA plus MAPK signaling pathway inhibitor obviously reduced release of NO. EDA may take effect with p38 MAPK, JNK and ERK inhibitors of sub-pathways in some way (s) to co-operate with EDA in modulating oxidative stress in activated microglia induced by LPS. As to the working mechanisms how EDA co-operates with MAPK inhibitors is still remain unknown.
- Edaravaone,
- Lipopolysaccharide,
- Microglia,
- Nitric oxide

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References(27)

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