Galangin Suppresses Pro-Inflammatory Gene Expression in Polyinosinic-Polycytidylic Acid-Stimulated Microglial Cells.
10.4062/biomolther.2017.173
- Author:
Min Ji CHOI
1
;
Jin Sun PARK
;
Jung Eun PARK
;
Han Su KIM
;
Hee Sun KIM
Author Information
1. Department of Molecular Medicine, Tissue Injury Defense Research Center, School of Medicine, Ewha Womans University, Seoul 07985, Republic of Korea. hskimp@ewha.ac.kr
- Publication Type:Original Article
- Keywords:
Galangin;
Poly(I:C);
Microglia;
PI3K/Akt;
NF-κB;
PPAR-γ signaling
- MeSH:
Alpinia;
Animals;
Brain;
Cytokines;
Gene Expression*;
Hand;
Honey;
In Vitro Techniques;
Interleukin-10;
Interleukin-6;
Interleukins;
Mice;
Microglia;
Negotiating;
Nitric Oxide;
Peroxisomes;
Phosphorylation;
Phosphotransferases;
Plants, Medicinal;
Poly I-C;
Reactive Oxygen Species;
Tumor Necrosis Factor-alpha;
Up-Regulation
- From:Biomolecules & Therapeutics
2017;25(6):641-647
- CountryRepublic of Korea
- Language:English
-
Abstract:
Galangin (3,5,7-trihydroxyflavone) is a polyphenolic compound abundant in honey and medicinal herbs, such as Alpinia officinarum. In this study, we investigated the anti-inflammatory effects of galangin under in vitro and in vivo neuroinflammatory conditions caused by polyinosinic-polycytidylic acid (poly(I:C)), a viral mimic dsRNA analog. Galangin suppressed the production of nitric oxide, reactive oxygen species, and pro-inflammatory cytokines in poly(I:C)-stimulated BV2 microglia. On the other hand, galangin enhanced anti-inflammatory interleukin (IL)-10 production. Galangin also suppressed the expression of pro-inflammatory markers in poly(I:C)-injected mouse brains. Further mechanistic studies showed that galangin inhibited poly(I:C)-induced nuclear factor (NF)-κB activity and phosphorylation of Akt without affecting MAP kinases. Interestingly, galangin increased the expression and transcriptional activity of peroxisome proliferator-activated receptor (PPAR)-γ, known to play an anti-inflammatory role. To investigate whether PPAR-γ is involved in the anti-inflammatory function of galangin, BV2 cells were pre-treated with PPAR-γ antagonist before treatment of galangin. We found that PPAR-γ antagonist significantly blocked galangin-mediated upregulation of IL-10 and attenuated the inhibition of tumor necrosis factor (TNF)-α and IL-6 in poly(I:C)-stimulated microglia. In conclusion, our data suggest that PI3K/Akt, NF-κB, and PPAR-γ play a pivotal role in mediating the anti-inflammatory effects of galangin in poly(I:C)-stimulated microglia.
