Protosappanin A exerts anti-neuroinflammatory effect by inhibiting JAK2-STAT3 pathway in lipopolysaccharide-induced BV2 microglia

作     者：WANG Li-Chao LIAO Li-Xi ZHAO Ming-Bo DONG Xin ZENG Ke-Wu TU Peng-Fei 

作者机构：State Key Laboratory of Natural and Biomimetic Drugs School of Pharmaceutical Sciences Peking University State Key Laboratory of Natural Medicines China Pharmaceutical University 

出 版 物：《Chinese Journal of Natural Medicines》 (中国天然药物（英文版）)

年 卷 期：2017年第15卷第9期

页      面：674-679页

核心收录：

学科分类：0710[理学-生物学] 1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 1005[医学-中医学] 100706[医学-药理学] 1002[医学-临床医学] 0703[理学-化学] 100602[医学-中西医结合临床] 10[医学] 

基　　金：supported by grants from the National Key Technology R&D Program "New Drug Innovation" of China(No.2012ZX09301002-002-002) the Natural Science Foundation of China(Nos.81303253 and 30873072) 

主　　题：Neuroinflammation BV2 microglia Lipopolysaccharide Protosappanin A JAK2-STAT3 

摘      要：Microglial activation and resultant neuroinflammatory response are implicated in various brain diseases including Alzheimer s disease and Parkinson s disease. Treatment with anti-neuroinflammatory agents could provide therapeutic benefits for such disorders. Protosappanin A(PTA) is a major bioactive ingredient isolated from Caesalpinia sappan L.. In this work, the anti-neuroinflammatory effects of PTA on LPS-stimulated BV2 cells were investigated and the underlying mechanisms were explored. Results showed that PTA significantly inhibited the production of TNF-α and IL-1β in LPS-activated BV2 microglia. Moreover, the mR NA expressions of IL-6, IL-1β, and MCP-1 were reduced by PTA in a dose-dependent manner. Furthermore, PTA suppressed JAK2/STAT3-dependent inflammation pathway through down-regulating the phosphorylation of JAK2 and STAT3, as well as STAT3 nuclear translocation against LPS treatment. These observations suggested a novel role for PTA in regulating LPS-induced neuroinflammatory injuries.