Aβ-induced microglial cell activation is inhibited by baicalin through the JAK2/STAT3 signaling pathway. (3rd August 2014)

• Record Type: Journal Article
• Authors: Xiong, Jiaxiang; Wang, Changzheng; Chen, Hongyan; Hu, Yazhuo; Tian, Lei; Pan, Jingkun; Geng, Miao
• Is Part Of: International journal of neuroscience. Volume 124:Number 8(2014:Aug.)
• Page Start: 609
• Page End: 620
• Publication Date: 2014-08-03
• Subjects: Nervous system -- Periodicals; 612.805
• DOI: 10.3109/00207454.2013.865027
• Languages: English
• ISSNs: 0020-7454

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p>Baicalin has shown multiple neuroprotective biological activities, including antiapoptotic and anti-inflammatory functions in neurodegeneration diseases. However, whether baicalin can regulate Aβ-induced microglial activation or inhibit inflammatory cytokine secretion has not been confirmed. We demonstrated that baicalin can inhibit beta amyloid peptides (Aβ42)-induced BV2 microglial cell proliferation, reduce the expression of CD11b, decrease chemotactic ability of BV2 cells and significantly inhibit the secretion of IL-6, TNF-α and NO. Moreover, baicalin pretreatment can effectively inhibit Aβ-induced phosphorylation of JAK2 and STAT3. Baicalin can inhibit Aβ-induced microglial cell activation by regulating the JAK2/STAT3 signaling pathway in AD transgenic mice. The modulation of microglial proliferation, activation and secretion by baicalin could be a promising therapeutic option for the treatment of Alzheimer's disease.</p> </abstract>