title: Curcumin attenuates the release of pro-inflammatory cytokines in lipopolysaccharide-stimulated BV2 microglia.
abstract: OBJECTIVE
  Pro-inflammatory mediators, such as prostaglandin E2 (PGE2) and nitric oxide (NO), and pro-inflammatory cytokines such as interleukin (IL)-1beta, IL-6, and TNF-alpha, play pivotal roles in brain injuries. The anti-inflammatory properties are known to be associated with significant reductions in pro-inflammatory mediators in brain injuries. In the present study we investigate whether the effects of curcumin on the production of pro-inflammatory mediators in lipopolysaccharide (LPS)-stimulated BV2 microglia.
  
  
  METHODS
  Curcumin were administered and their effects on LPS-induced pro-inflammatory mediators were monitored by Western blotting and RT-PCR.
  
  
  RESULTS
  Curcumin significantly inhibited the release of NO, PGE2, and pro-inflammatory cytokines in a dose-dependent manner. Curcumin also attenuated the expressions of inducible NO synthase and cyclooxygenase-2 mRNA and protein levels. Moreover, curcumin suppressed NF-kappaB activation via the translocation of p65 into the nucleus. Our data also indicate that curcumin exerts anti-inflammatory properties by suppressing the transcription of proinflammatory cytokine genes through the NF-kappaB signaling pathway.
  
  
  CONCLUSIONS
  Anti-inflammatory properties of curcumin may be useful for treating the inflammatory and deleterious effects of microglial activation in response to LPS stimulation.
authors: Department of Microbiology, College of Natural Sciences, Pusan National University, Busan 609-735, Korea.
authors: Cheng-Yun
authors: CY
authors: Jin
authors: Jae-Dong
authors: JD
authors: Lee
authors: Cheol
authors: C
authors: Park
authors: Yung-Hyun
authors: YH
authors: Choi
authors: Gi-Young
authors: GY
authors: Kim
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000494:pharmacology; D015153:Blotting, Western; D002460:Cell Line; D003474:Curcumin / Q000008:administration & dosage / Q000494:pharmacology*; D051546:Cyclooxygenase 2 / Q000096:biosynthesis* / Q000235:genetics; D016207:Cytokines / Q000378:metabolism; D015232:Dinoprostone / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D017628:Microglia / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009569:Nitric Oxide / Q000096:biosynthesis; D052247:Nitric Oxide Synthase Type II / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D008070:Lipopolysaccharides; D016328:NF-kappa B; D012333:RNA, Messenger; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D003474:Curcumin; D015232:Dinoprostone