Chlorogenic acid inhibits LPS-induced microglial activation and improves survival of dopaminergic neurons

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• 作者：Wenjuan Shen^a ; ^b ; ^c ; Renbin Qi^a ; ^b ; ^c ; Jing Zhang^a ; ^b ; ^c ; Zhigang Wang^a ; ^b ; ^c ; Huadong Wang^a ; ^b ; ^c ; Chaofeng Hu^a ; ^b ; ^c ; Yanru Zhao^a ; ^b ; ^c ; Man Bie^a ; ^b ; ^c ; Yanping Wang^a ; ^b ; ^c ; Yongmei Fu^a ; ^b ; ^c ; Mengfei Chen^d ; Daxiang Lu^a ; ^b ; ^c ; ^{ldx@jnu.edu.cn}
• 关键词：Chlorogenic acid ; Lipopolysaccharide ; Microglia ; Neuroinflammation ; Nuclear factor-魏B
• 刊名：Brain Research Bulletin
• 出版年：2012
• 期刊代码：9_03619230
• 类别：neu
• 出版时间：1 August, 2012
• 卷：88
• 期：5
• 页码：487-494
• 文件大小：949 K

摘要

Pro-inflammatory factors released by activated microglia may contribute to the progression of neurodegenerative diseases. As a natural phenolic acid, chlorogenic acid (CGA) has been shown to have anti-inflammatory properties. However, it is unclear whether CGA has the ability to mediate microglial activation. The present study investigated the role of CGA in lipopolysaccharide (LPS)-stimulated microglia. Our data demonstrated that CGA significantly suppressed NO production and TNF-伪 release in LPS-stimulated primary microglia. In addition, CGA decreased LPS-stimulated phosphorylation and degradation of inhibitory kappa B-alpha (I魏B伪), and prevented translocation of nuclear factor-kappaB (NF-魏B). Furthermore, CGA prevented neurotoxicity caused by microglial activation and ultimately improved survival of dopaminergic (DA) neuron. Finally, in vivo data showed that CGA pretreatment attenuated LPS-induced IL-1尾 and TNF-伪 release in substantia nigra (SN). Our results suggested that the pretreatment of CGA significantly inhibits the microglial activation, and CGA may be neuroprotective for pro-inflammatory factor-mediated neurodegenerative disorders.