Cyclosporin-A inhibits the expression of cyclooxygenase-2 in gingiva
Identifieur interne : 006B32 ( Main/Exploration ); précédent : 006B31; suivant : 006B33Cyclosporin-A inhibits the expression of cyclooxygenase-2 in gingiva
Auteurs : C. Y. Chiang [Taïwan] ; Y.-T. Chen [Taïwan] ; F.-M. Hung [Taïwan] ; H.-P. Tu [Taïwan] ; M. M.-J. Fu [Taïwan] ; E. Fu [Taïwan]Source :
- Journal of periodontal research [ 0022-3484 ] ; 2007.
Descripteurs français
- KwdFr :
- Adulte, Animaux, Antienzymes (pharmacologie), Cellules cultivées, Cellules stromales (), Cellules stromales (enzymologie), Cellules épithéliales (), Cellules épithéliales (enzymologie), Ciclosporine (pharmacologie), Cyclooxygenase 2 (analyse), Dinoprostone (analyse), Facteur de nécrose tumorale alpha (analyse), Femelle, Fibroblastes (), Fibroblastes (enzymologie), Gencive (), Gencive (enzymologie), Humains, Inhibiteurs de la cyclooxygénase 2 (pharmacologie), Interleukine-1 bêta (analyse), Interleukine-6 (analyse), Mâchoire édentée (anatomopathologie), RT-PCR, Rat Sprague-Dawley, Rats, Technique de Western.
- MESH :
- analyse : Cyclooxygenase 2, Dinoprostone, Facteur de nécrose tumorale alpha, Interleukine-1 bêta, Interleukine-6.
- anatomopathologie : Mâchoire édentée.
- enzymologie : Cellules stromales, Cellules épithéliales, Fibroblastes, Gencive.
- pharmacologie : Antienzymes, Ciclosporine, Inhibiteurs de la cyclooxygénase 2.
- Pascal (Inist)
English descriptors
- KwdEn :
- Adult, Animals, Blotting, Western, Cells, Cultured, Ciclosporin, Cyclooxygenase 2, 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, Gingiva (drug effects), Gingiva (enzymology), Humans, Immunosuppressive agent, Interleukin-1beta (analysis), Interleukin-6 (analysis), Jaw, Edentulous (pathology), Prostaglandin-endoperoxide synthase, Rats, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction, Secondary effect, Stomatology, Stromal Cells (drug effects), Stromal Cells (enzymology), Tumor Necrosis Factor-alpha (analysis).
- MESH :
- chemical , analysis : Cyclooxygenase 2, Dinoprostone, Interleukin-1beta, Interleukin-6, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Cyclooxygenase 2 Inhibitors, Cyclosporine, Enzyme Inhibitors.
- drug effects : Epithelial Cells, Fibroblasts, Gingiva, Stromal Cells.
- enzymology : Epithelial Cells, Fibroblasts, Gingiva, Stromal Cells.
- pathology : Jaw, Edentulous.
- Adult, Animals, Blotting, Western, Cells, Cultured, Female, Humans, Rats, Rats, Sprague-Dawley, Reverse Transcriptase Polymerase Chain Reaction.
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-1β mRNA, tumor necrosis factor-α 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-1β 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 non-retentive 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.
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">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-1β mRNA, tumor necrosis factor-α mRNA, and interleukin-6 mRNA was examined in the edentulous gingiva. The expression of cyclooxygenase-2 protein and the production of prostaglandin E<sub>2</sub>
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-1β 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 E<sub>2</sub>
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 non-retentive 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.</div>
</front>
</TEI>
<affiliations><list><country><li>Taïwan</li>
</country>
</list>
<tree><country name="Taïwan"><noRegion><name sortKey="Chiang, C Y" sort="Chiang, C Y" uniqKey="Chiang C" first="C. Y." last="Chiang">C. Y. Chiang</name>
</noRegion>
<name sortKey="Chen, Y T" sort="Chen, Y T" uniqKey="Chen Y" first="Y.-T." last="Chen">Y.-T. Chen</name>
<name sortKey="Fu, E" sort="Fu, E" uniqKey="Fu E" first="E." last="Fu">E. Fu</name>
<name sortKey="Fu, M M J" sort="Fu, M M J" uniqKey="Fu M" first="M. M.-J." last="Fu">M. M.-J. Fu</name>
<name sortKey="Fu, M M J" sort="Fu, M M J" uniqKey="Fu M" first="M. M.-J." last="Fu">M. M.-J. Fu</name>
<name sortKey="Hung, F M" sort="Hung, F M" uniqKey="Hung F" first="F.-M." last="Hung">F.-M. Hung</name>
<name sortKey="Hung, F M" sort="Hung, F M" uniqKey="Hung F" first="F.-M." last="Hung">F.-M. Hung</name>
<name sortKey="Tu, H P" sort="Tu, H P" uniqKey="Tu H" first="H.-P." last="Tu">H.-P. Tu</name>
<name sortKey="Tu, H P" sort="Tu, H P" uniqKey="Tu H" first="H.-P." last="Tu">H.-P. Tu</name>
</country>
</tree>
</affiliations>
</record>
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