Cyclosporin-A inhibits the expression of cyclooxygenase-2 in gingiva

J Periodontal Res. 2007 Oct;42(5):443-9. doi: 10.1111/j.1600-0765.2006.00967.x.

Abstract

Background and objective: Various inflammatory mediators are involved in the development of cyclosporine A-induced gingival overgrowth. In this study, the gingival expression of cyclooxygenase-2 after cyclosporine A therapy was examined in vivo and in vitro.

Material and methods: After edentulous ridges on maxilla were established, 21 Sprague-Dawley rats received cyclosporine A daily for 4 wk, and a further 21 rats received solvent. After the rats were killed, the expression of cyclooxygenase-2 mRNA, interleukin-1beta mRNA, tumor necrosis factor-alpha mRNA, and interleukin-6 mRNA was examined in the edentulous gingiva. The expression of cyclooxygenase-2 protein and the production of prostaglandin E2 were also evaluated.

Results: In cultured human gingival fibroblasts and epithelial cells, the expression of cyclooxygenase-2 mRNA was measured after treatment with cyclosporine A. Significantly lower expression of cyclooxygenase-2 and interleukin-1beta mRNA, but higher interleukin-6 expression, were observed in gingiva from cyclosporine A-treated rats than in those from the control rats. Significantly less prostaglandin E2 production was observed in cyclosporine A-treated rats. Immunohistochemistry revealed that fewer gingival stromal cells were positively stained for cyclooxygenase-2 in cyclosporine A-treated rats. In cultured cells, significantly less cyclooxygenase-2 mRNA was detected after treatment with cyclosporine A.

Conclusion: The expression of cyclooxygenase-2 was lower in the plaque nonretentive gingivae and the in vitro gingival cells upon treatment with cyclosporine A. Thus, we propose that cyclosporine A inhibits the expression of gingival cyclooxygenase-2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Animals
  • Blotting, Western
  • Cells, Cultured
  • Cyclooxygenase 2 / analysis
  • Cyclooxygenase 2 Inhibitors / pharmacology*
  • Cyclosporine / pharmacology*
  • Dinoprostone / analysis
  • Enzyme Inhibitors / pharmacology*
  • Epithelial Cells / drug effects
  • Epithelial Cells / enzymology
  • Female
  • Fibroblasts / drug effects
  • Fibroblasts / enzymology
  • Gingiva / drug effects
  • Gingiva / enzymology*
  • Humans
  • Interleukin-1beta / analysis
  • Interleukin-6 / analysis
  • Jaw, Edentulous / pathology
  • Rats
  • Rats, Sprague-Dawley
  • Reverse Transcriptase Polymerase Chain Reaction
  • Stromal Cells / drug effects
  • Stromal Cells / enzymology
  • Tumor Necrosis Factor-alpha / analysis

Substances

  • Cyclooxygenase 2 Inhibitors
  • Enzyme Inhibitors
  • Interleukin-1beta
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Cyclosporine
  • Cyclooxygenase 2
  • Dinoprostone