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Galangin suppresses pro-inflammatory gene expression in polyinosinic-polycytidylic acid-stimulated microglial cells
- Galangin suppresses pro-inflammatory gene expression in polyinosinic-polycytidylic acid-stimulated microglial cells
- Choi M.-J.; Park J.-S.; Park J.-E.; Kim H.S.; Kim H.-S.
- Ewha Authors
- 김희선; 김한수
- SCOPUS Author ID
- 김희선; 김한수
- Issue Date
- Journal Title
- Biomolecules and Therapeutics
- Biomolecules and Therapeutics vol. 25, no. 6, pp. 641 - 647
- Galangin; Microglia; NF-κB; PI3K/Akt; Poly(I:C); PPAR-γ signaling
- Korean Society of Applied Pharmacology
- SCIE; SCOPUS; KCI
- Document Type
- 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. © 2017 The Korean Society of Applied Pharmacology.
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