title: Quest for anti-inflammatory substances using IL-1β-stimulated gingival fibroblasts.
abstract: BACKGROUND
  We have previously reported that azulene-related compounds, and alkaline extract of Sasa senanensis Rehder potently inhibited nitric oxide (NO) production by lipopolysaccharide (LPS)-stimulated mouse macrophages. We investigated here whether they can inhibit pro-inflammatory cytokine production, by activated human gingival fibroblast (HGF).
  
  
  METHODS
  HGF was established from the periodontal tissues of extracted tooth. Viable cell number was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. Production of Prostaglandin E(2) (PGE(2)) and cytokines was determined by enzyme immunoassay, and enzyme-linked immunosorbent assay, respectively.
  
  
  RESULTS
  Interleukin (IL)-1β did not inhibit, but rather slightly stimulated the growth of HGF cells. IL-1β stimulated the production of PGE(2), IL-6, IL-8 and monocyte chemotactic protein-1 very potently, but not that of nitric oxide and tumor necrosis factor-α. Native LPS and synthetic lipid A from E. coli and P. gingivalis was much less stimulatory. Dexamethasone, not indomethacin, was an efficient inhibitor of IL-8 production. Among five azulene-related compounds, benzo[b]cyclohepta[e][1,4]thiazine most potently inhibited the IL-8 production by HGF cells, as well as NO production by activated RAW264.7 cells. The alkaline extract of Sasa senanensis Rehder significantly inhibited IL-8 production, without affecting the cell viability.
  
  
  CONCLUSIONS
  The present system may be applicable for use in the search for anti-gingivitis substances.
authors.affiliation: Faculty of Science, Josai University, Sakado, Saitama 350-0295, Japan.
authors.forename: Manami
authors.initials: M
authors.lastname: Ono
authors.forename: Kaori
authors.initials: K
authors.lastname: Kantoh
authors.forename: Junichi
authors.initials: J
authors.lastname: Ueki
authors.forename: Aki
authors.initials: A
authors.lastname: Shimada
authors.forename: Hidetsugu
authors.initials: H
authors.lastname: Wakabayashi
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Matsuta
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Sakagami
authors.forename: Hidefumi
authors.initials: H
authors.lastname: Kumada
authors.forename: Nobushiro
authors.initials: N
authors.lastname: Hamada
authors.forename: Madoka
authors.initials: M
authors.lastname: Kitajima
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Oizumi
authors.forename: Takaaki
authors.initials: T
authors.lastname: Oizumi
mesh_terms: D000893:Anti-Inflammatory Agents / Q000302:isolation & purification / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology; D045744:Cell Line, Tumor; D002850:Chromatography, Gel; D004353:Drug Evaluation, Preclinical; D004357:Drug Synergism; D005347:Fibroblasts / Q000187:drug effects*; D005881:Gingiva / Q000473:pathology*; D006801:Humans; D053583:Interleukin-1beta / Q000494:pharmacology* / Q000502:physiology; D010936:Plant Extracts / Q000302:isolation & purification / Q000494:pharmacology*; D018515:Plant Leaves / Q000737:chemistry; D011837:Radiation-Protective Agents / Q000302:isolation & purification / Q000494:pharmacology; D031787:Sasa / Q000737:chemistry; D014466:Ultraviolet Rays
chemical_list: D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D053583:Interleukin-1beta; D010936:Plant Extracts; D011837:Radiation-Protective Agents; D001205:Ascorbic Acid