title: Ozonated water improves lipopolysaccharide-induced responses of an odontoblast-like cell line.
abstract: BACKGROUND
  It is important to develop an antimicrobial agent without any damage on dental pulp. In the present study, we examined whether pretreatment of bacterial lipopolysaccharides (LPS) with ozonated water (O(3)aq) improves LPS-induced responses of rat odontoblastic cell line, KN-3.
  
  
  METHODS
  After the pretreatment of LPS with O(3)aq, effects of LPS and O(3)aq-treated LPS on cell viability; calcification ability; expression of cyclooxygenase 2 (COX-2), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNF-alpha); and activation of p38 of KN-3 cells were examined.
  
  
  RESULTS
  The formation of mineralized nodules by KN-3 cells was suppressed by LPS, whereas that suppression was inhibited by the pretreatment of LPS with ozonated water. We also found that LPS-induced expression of COX-2, IL-6, and TNF-alpha and p38 activation were markedly suppressed when LPS was pretreated with ozonated water. Furthermore, expression of COX-2, IL-6, and TNF-alpha by LPS were mainly induced through p38 activation.
  
  
  CONCLUSIONS
  These results suggest that odontoblastic cells exhibit inflammatory responses against LPS and that ozonated water has the ability to improve LPS-induced inflammatory responses and suppression of odontoblastic properties of KN-3 cells through direct inhibition of LPS.
authors.affiliation: Department of Cariology and Periodontology, Division of Pulp Biology, Operative Dentistry, and Endodontics, Kyushu Dental College, Kitakyushu, Japan.
authors.forename: Fumiko
authors.initials: F
authors.lastname: Noguchi
authors.forename: Chiaki
authors.initials: C
authors.lastname: Kitamura
authors.forename: Masato
authors.initials: M
authors.lastname: Nagayoshi
authors.forename: Ker-Kong
authors.initials: KK
authors.lastname: Chen
authors.forename: Masamichi
authors.initials: M
authors.lastname: Terashita
authors.forename: Tatsuji
authors.initials: T
authors.lastname: Nishihara
mesh_terms: D016976:Aggregatibacter actinomycetemcomitans; D000818:Animals; D000890:Anti-Infective Agents / Q000494:pharmacology*; D002070:Butadienes / Q000494:pharmacology; D002113:Calcification, Physiologic / Q000187:drug effects; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D051545:Cyclooxygenase 1 / Q000187:drug effects; D051546:Cyclooxygenase 2 / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004926:Escherichia coli; D007093:Imidazoles / Q000494:pharmacology; D015850:Interleukin-6 / Q000032:analysis; D008050:Lipid A / Q000037:antagonists & inhibitors; D008070:Lipopolysaccharides / Q000037:antagonists & inhibitors*; D008565:Membrane Proteins / Q000187:drug effects; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000187:drug effects; D009570:Nitriles / Q000494:pharmacology; D009804:Odontoblasts / Q000187:drug effects*; D010083:Oxidants, Photochemical / Q000494:pharmacology*; D010126:Ozone / Q000494:pharmacology*; D010766:Phosphorylation / Q000187:drug effects; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D014409:Tumor Necrosis Factor-alpha / Q000187:drug effects; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000187:drug effects
chemical_list: D000890:Anti-Infective Agents; D002070:Butadienes; D004791:Enzyme Inhibitors; D007093:Imidazoles; D015850:Interleukin-6; D008050:Lipid A; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D009570:Nitriles; D010083:Oxidants, Photochemical; D011725:Pyridines; D014409:Tumor Necrosis Factor-alpha; C113580:U 0126; D010126:Ozone; D051545:Cyclooxygenase 1; D051546:Cyclooxygenase 2; C496513:Ptgs1 protein, rat; C489691:Ptgs2 protein, rat; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; C093642:SB 203580