title: Ketoprofen inhibits expression of inflammatory mediators in human dental pulp cells.
abstract: BACKGROUND
  Conventional root canal treatment is the treatment of choice for the irreversible pulpitis caused by bacterial infection. More recently, vital pulp therapy has been proposed as an alternative for management of inflamed dental pulp. Ketoprofen is an anti-inflammatory agent commonly used as a component of mouth rinse for oral lesions. Here, we examined the effect and mechanisms of action of ketoprofen on the expression of inflammatory mediators induced by the lipopolysaccharide (LPS) in dental pulp cells.
  
  
  METHODS
  Human dental pulp cells were exposed to LPS or LPS + ketoprofen, and reverse-transcription polymerase chain reaction was used to detect interleukin-1β and tumor necrosis factor α. The effect of these treatments on mitogen-activated protein kinase pathways was assessed by Western blots for extracellular signal-regulated kinase and c-Jun N-terminal kinase.
  
  
  RESULTS
  LPS induced interleukin-1β and tumor necrosis factor α in dental pulp cells. Ketoprofen effectively inhibited interleukin-1β and tumor necrosis factor α production in LPS-stimulated dental pulp cells. Notably, ketoprofen inhibited phosphorylation of extracellular signal-regulated kinase and c-Jun N-terminal kinase.
  
  
  CONCLUSIONS
  Ketoprofen inhibited expression inflammatory mediators in dental pulp cells stimulated with LPS. The inhibitory effect of ketoprofen on inflammatory cytokines is associated with inhibition of the mitogen-activated protein kinase pathway.
authors.affiliation: School of Dentistry, Dental Science Research Institute, Chonnam National University, Gwangju, Korea.
authors.forename: Eun-Kyoung
authors.initials: EK
authors.lastname: Choi
authors.forename: Sun-Ho
authors.initials: SH
authors.lastname: Kim
authors.forename: In-Chol
authors.initials: IC
authors.lastname: Kang
authors.forename: Ji-Yeon
authors.initials: JY
authors.lastname: Jeong
authors.forename: Jeong-Tae
authors.initials: JT
authors.lastname: Koh
authors.forename: Bin-Na
authors.initials: BN
authors.lastname: Lee
authors.forename: Won-Mann
authors.initials: WM
authors.lastname: Oh
authors.forename: Kyung-San
authors.initials: KS
authors.lastname: Min
authors.forename: Jacques E
authors.initials: JE
authors.lastname: Nör
authors.forename: Yun-Chan
authors.initials: YC
authors.lastname: Hwang
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D018929:Cell Culture Techniques; D002478:Cells, Cultured; D003782:Dental Pulp / Q000187:drug effects* / Q000473:pathology; D004926:Escherichia coli; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors / Q000187:drug effects; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis / Q000037:antagonists & inhibitors*; D053583:Interleukin-1beta / Q000037:antagonists & inhibitors / Q000187:drug effects; D048031:JNK Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000187:drug effects; D007660:Ketoprofen / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000009:adverse effects; D020935:MAP Kinase Signaling System / Q000187:drug effects; D010766:Phosphorylation; D016966:Porphyromonas gingivalis; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000187:drug effects
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018836:Inflammation Mediators; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D007660:Ketoprofen; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases