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

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          Abstract

          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-1 β in LPS-activated BV2 microglia. Moreover, the mRNA expressions of IL-6, IL-1 β, 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.

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          Author and article information

          Journal
          CJNM
          Chinese Journal of Natural Medicines
          Elsevier
          1875-5364
          20 September 2017
          : 15
          : 9
          : 674-679
          Affiliations
          1State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China
          2State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China
          Author notes
          *Corresponding author: ZENG Ke-Wu, E-mail: ZKW@ 123456bjmu.edu.cn ; TU Peng-Fei E-mail: pengfeitu@ 123456vip.163.com

          These authors have no conflict of interest to declare.

          Article
          S1875-5364(17)30096-1
          10.1016/S1875-5364(17)30096-1
          Copyright © 2017 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
          Funding
          Funded by: National Key Technology R & D Program “New Drug Innovation” of China
          Award ID: 2012ZX09301002-002-002
          Funded by: Natural Science Foundation of China
          Award ID: 81303253
          Award ID: 30873072
          This work was supported by grants from the National Key Technology R & D Program “New Drug Innovation” of China (No. 2012ZX09301002-002-002) and the Natural Science Foundation of China (Nos. 81303253 and 30873072).

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