Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김희선 | * |
dc.contributor.author | 박은미 | * |
dc.date.accessioned | 2017-12-27T16:31:10Z | - |
dc.date.available | 2017-12-27T16:31:10Z | - |
dc.date.issued | 2017 | * |
dc.identifier.issn | 0006-2952 | * |
dc.identifier.other | OAK-21399 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/239430 | - |
dc.description.abstract | Since microglia-associated neuroinflammation plays a pivotal role in the progression of neurodegenerative diseases, controlling microglial activation has been suggested as a potential therapeutic strategy. Here, we investigated the anti-inflammatory effects of galangin (3,5,7-trihydroxyflavone) in microglia and analyzed the underlying molecular mechanisms. Galangin inhibited the expression of inducible nitric oxide synthase (iNOS) and pro-inflammatory cytokines and enhanced the expression of anti-inflammatory interleukin (IL)-10 in lipopolysaccharide (LPS)-stimulated BV2 microglia. Galangin also suppressed microglial activation and the expression of pro-inflammatory markers in LPS-injected mouse brains. The results of mechanistic studies have shown that galangin inhibited LPS-induced phosphorylation of p38 mitogen activated protein kinase (MAPK), c-Jun N-terminal kinase (JNK), phosphatidylinositol 3-kinase (PI3K)/Akt, and nuclear factor (NF)-κB activity. On the contrary, galangin increased the activity of transcription factors, such as nuclear factor-E2-related factor 2 (Nrf2), cAMP response element-binding protein (CREB), and peroxisome proliferator-activated receptor (PPAR)-γ, known to play an anti-inflammatory role. In addition, galangin showed antioxidant effects by suppressing the expression of NADPH oxidase subunits p47phox and gp91phox, and by enhancing hemeoxygenase-1. We then investigated whether PPAR-γ was involved in the anti-inflammatory function of galangin. Pretreatment with a PPAR-γ antagonist or siRNA significantly blocked galangin-mediated upregulation of IL-10 and attenuated the inhibition of tumor necrosis factor (TNF)-α, nitric oxide (NO), and IL-6 in LPS-stimulated microglia. Moreover, the PPAR-γ antagonist reversed the effects of galangin on NF-κB, Nrf2, and CREB. Altogether, our data suggest that PPAR-γ plays a key role in mediating the anti-inflammatory effects of galangin by modulating the NF-κB and Nrf2/CREB signaling pathways. © 2017 Elsevier Inc. | * |
dc.language | English | * |
dc.publisher | Elsevier Inc. | * |
dc.subject | Galangin | * |
dc.subject | Neuroinflammation | * |
dc.subject | NF-κB | * |
dc.subject | Nrf2/CREB signaling | * |
dc.subject | PPAR-γ | * |
dc.title | Anti-inflammatory mechanism of galangin in lipopolysaccharide-stimulated microglia: Critical role of PPAR-γ signaling pathway | * |
dc.type | Article | * |
dc.relation.volume | 144 | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 120 | * |
dc.relation.lastpage | 131 | * |
dc.relation.journaltitle | Biochemical Pharmacology | * |
dc.identifier.doi | 10.1016/j.bcp.2017.07.021 | * |
dc.identifier.wosid | WOS:000413611500011 | * |
dc.identifier.scopusid | 2-s2.0-85026645367 | * |
dc.author.google | Choi M.-J. | * |
dc.author.google | Lee E.-J. | * |
dc.author.google | Park J.-S. | * |
dc.author.google | Kim S.-N. | * |
dc.author.google | Park E.-M. | * |
dc.author.google | Kim H.-S. | * |
dc.contributor.scopusid | 김희선(57191372551) | * |
dc.contributor.scopusid | 박은미(35933416400) | * |
dc.date.modifydate | 20240123095000 | * |