title: Piceatannol attenuates lipopolysaccharide-induced NF-kappaB activation and NF-kappaB-related proinflammatory mediators in BV2 microglia.
abstract: Proinflammatory mediators, such as prostaglandin E(2) (PGE(2)), nitric oxide (NO), and proinflammatory cytokines [interlukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha] play pivotal roles in brain injuries. Anti-inflammatory responses are associated with significant downregulation of these proinflammatory mediators following brain injury. In the present study, we investigated the effects of piceatannol (PIC) on the production of proinflammatory mediators in lipopolysaccharide (LPS)-stimulated BV2 microglia. PIC significantly inhibited the release of NO, PGE(2), and proinflammatory cytokines in a dose-dependent manner. PIC also attenuated the expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 mRNA and protein levels. Moreover, PIC prevented NF-kappaB p65 nuclear translocation. Our data also indicate that PIC exhibits anti-inflammatory properties by suppressing the transcription of proinflammatory cytokine genes through the NF-kappaB signaling pathway. The anti-inflammatory properties of PIC may be useful for attenuating inflammatory diseases and LPS-stimulated microglial activation.
authors.affiliation: Department of Microbiology, College of Natural Sciences, Pusan National University, Busan 609-735, South Korea.
authors.forename: Cheng-Yun
authors.initials: CY
authors.lastname: Jin
authors.forename: Dong-Oh
authors.initials: DO
authors.lastname: Moon
authors.forename: Kyeong-Jun
authors.initials: KJ
authors.lastname: Lee
authors.forename: Mun-Ok
authors.initials: MO
authors.lastname: Kim
authors.forename: Jae-Dong
authors.initials: JD
authors.lastname: Lee
authors.forename: Yung Hyun
authors.initials: YH
authors.lastname: Choi
authors.forename: Yeong-Min
authors.initials: YM
authors.lastname: Park
authors.forename: Gi-Young
authors.initials: GY
authors.lastname: Kim
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D018836:Inflammation Mediators / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008156:Luciferases / Q000096:biosynthesis; D051379:Mice; D017628:Microglia / Q000187:drug effects*; D016328:NF-kappa B / Q000187:drug effects / Q000502:physiology*; D009569:Nitric Oxide / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis; D009573:Nitrites / Q000032:analysis / Q000378:metabolism; D012313:RNA / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013267:Stilbenes / Q000494:pharmacology*
chemical_list: D016207:Cytokines; D004791:Enzyme Inhibitors; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; D009573:Nitrites; D013267:Stilbenes; D009569:Nitric Oxide; D012313:RNA; C041525:3,3',4,5'-tetrahydroxystilbene; D008156:Luciferases; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D015232:Dinoprostone