The expression of 11β-hydroxysteroid dehydrogenase type 1 is increased in experimental periodontitis in rats

書誌事項

タイトル
The expression of 11β-hydroxysteroid dehydrogenase type 1 is increased in experimental periodontitis in rats
タイトル別名
  • ラットの実験的歯周炎において11β-hydroxysteroid dehydrogenase type 1の発現が増加する
著者
中田, 貴也
学位授与大学
大阪歯科大学
取得学位
博士(歯学)
学位授与番号
甲第788号
学位授与年月日
2017-03-10

説明

The involvement of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which converts inactive glucocorticoids into active glucocorticoids intracellularly, in metabolic diseases and chronic inflammatory diseases has been elucidated. To clarify the role of 11β-HSD1 in chronic periodontitis, the expression of 11β-HSD1 was investigated in an experimental periodontitis model in rats. Experimental periodontitis was induced by silk ligature. The expression of 11β-HSD1 was examined using real time PCR. The expression of 11β-HSD1 mRNA was significantly increased in experimental periodontitis compared with the control. This result suggests that the increased expression of 11β-HSD1, which results in increased levels of intracellular glucocorticoids, may play a role in the pathophysiology of experimental periodontitis.

2016年度

収集根拠 : 博士論文(自動収集)
資料形態 : テキストデータ
コレクション : 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
The involvement of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which converts inactive glucocorticoids into active glucocorticoids intracellularly, in metabolic diseases and chronic inflammatory diseases has been elucidated. To clarify the role of 11β-HSD1 in chronic periodontitis, the expression of 11β-HSD1 was investigated in an experimental periodontitis model in rats. Experimental periodontitis was induced by silk ligature. The expression of 11β-HSD1 was examined using real time PCR. The expression of 11β-HSD1 mRNA was significantly increased in experimental periodontitis compared with the control. This result suggests that the increased expression of 11β-HSD1, which results in increased levels of intracellular glucocorticoids, may play a role in the pathophysiology of experimental periodontitis.
2016年度

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