Protosappanin A exerts anti-neuroinflammatory effect by inhibiting JAK2-STAT3 pathway in lipopolysaccharide-induced BV2 microglia.
10.1016/S1875-5364(17)30096-1
- Author:
Li-Chao WANG
1
,
2
;
Li-Xi LIAO
3
;
Ming-Bo ZHAO
3
;
Xin DONG
3
;
Ke-Wu ZENG
4
;
Peng-Fei TU
1
,
5
Author Information
1. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China
2. State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China.
3. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China.
4. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China. Electronic address: ZKW@bjmu.edu.cn.
5. State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, China. Electronic address: pengfeitu@vip.163.com.
- Publication Type:Journal Article
- Keywords:
BV2 microglia;
JAK2-STAT3;
Lipopolysaccharide;
Neuroinflammation;
Protosappanin A
- MeSH:
Animals;
Anti-Inflammatory Agents;
pharmacology;
Humans;
Inflammation;
drug therapy;
genetics;
immunology;
Interleukin-1beta;
genetics;
immunology;
Lipopolysaccharides;
pharmacology;
Mice;
Microglia;
drug effects;
immunology;
Nitric Oxide;
genetics;
immunology;
Phenols;
pharmacology;
STAT3 Transcription Factor;
genetics;
immunology;
Signal Transduction;
drug effects;
Tumor Necrosis Factor-alpha;
genetics;
immunology
- From:
Chinese Journal of Natural Medicines (English Ed.)
2017;15(9):674-679
- CountryChina
- Language:English
-
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-1β in LPS-activated BV2 microglia. Moreover, the mRNA 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.
