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http://purl.uniprot.org/citations/28254441http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28254441http://www.w3.org/2000/01/rdf-schema#comment"Obesity and diabetes are known risk factors for dementia, and it is speculated that chronic neuroinflammation contributes to this increased risk. Microglia are brain-resident immune cells modulating the neuroinflammatory state. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the major ω-3 polyunsaturated fatty acids (PUFAs) of fish oil, exhibit various effects, which include shifting microglia to the anti-inflammatory phenotype. To identify the molecular mechanisms involved, we examined the impact of EPA, DHA, and EPA+DHA on the lipopolysaccharide (LPS)-induced cytokine profiles and the associated signaling pathways in the mouse microglial line MG6. Both EPA and DHA suppressed the production of the pro-inflammatory cytokines TNF-α and IL-6 by LPS-stimulated MG6 cells, and this was also observed in LPS-stimulated BV-2 cells, the other microglial line. Moreover, the EPA+DHA mixture activated SIRT1 signaling by enhancing mRNA level of nicotinamide phosphoribosyltransferase (NAMPT), cellular NAD+ level, SIRT1 protein deacetylase activity, and SIRT1 mRNA levels in LPS-stimulated MG6. EPA+DHA also inhibited phosphorylation of the stress-associated transcription factor NF-κB subunit p65 at Ser536, which is known to enhance NF-κB nuclear translocation and transcriptional activity, including cytokine gene activation. Further, EPA+DHA increased the LC3-II/LC3-I ratio, an indicator of autophagy. Suppression of TNF-α and IL-6 production, inhibition of p65 phosphorylation, and autophagy induction were abrogated by a SIRT1 inhibitor. On the other hand, NAMPT inhibition reversed TNF-α suppression but not IL-6 suppression. Accordingly, these ω-3 PUFAs may suppress neuroinflammation through SIRT1-mediated inhibition of the microglial NF-κB stress response and ensue pro-inflammatory cytokine release, which is implicated in NAMPT-related and -unrelated pathways."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.org/dc/terms/identifier"doi:10.1016/j.bbalip.2017.02.010"xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Inoue T."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Hasegawa K."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Masuda S."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Tanaka M."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Wada H."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Kusakabe T."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Shimatsu A."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Muranaka K."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Yamakage H."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Satoh-Asahara N."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/author"Ohue-Kitano R."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/name"Biochim Biophys Acta Mol Cell Biol Lipids"xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/pages"552-560"xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/title"Omega-3 polyunsaturated fatty acids suppress the inflammatory responses of lipopolysaccharide-stimulated mouse microglia by activating SIRT1 pathways."xsd:string
http://purl.uniprot.org/citations/28254441http://purl.uniprot.org/core/volume"1862"xsd:string
http://purl.uniprot.org/citations/28254441http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/28254441
http://purl.uniprot.org/citations/28254441http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/28254441
http://purl.uniprot.org/uniprot/#_A7MCT8-mappedCitation-28254441http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28254441
http://purl.uniprot.org/uniprot/#_F6YAQ3-mappedCitation-28254441http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28254441
http://purl.uniprot.org/uniprot/#_Q3USY7-mappedCitation-28254441http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28254441
http://purl.uniprot.org/uniprot/#_Q53Z05-mappedCitation-28254441http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/28254441