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- Sakoda Kenji
- Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences
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- Yamamoto Matsuo
- Department of Periodontology, School of Dentistry, Showa University
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- Negishi Yoichi
- School of Pharmacy, Tokyo University of Pharmacy and Life Sciences
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- Liao James K
- Vascular Medicine Unit, Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, U.S.A.
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- Node Koichi
- Department of Cardiovascular & Renal Medicine, Saga University Faculty of Medicine
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- Izumi Yuichi
- Department of Periodontology, Kagoshima University Graduate School of Medical and Dental Sciences
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Periodontitis is a chronic inflammatory disease associated with degradation of periodontal tissues and is highly prevalent in late middle age.<BR>Statins, such as simvastatin, are pharmacologic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors that inhibit cholesterol synthesis, which is important in development of arteriosclerosis. Many cardiovascular studies have suggested that statins also have anti-inflammatory effects which are independent of cholesterol lowering. As a chronic inflammatory disease, periodontitis shares some mechanisms with atherosclerosis. Since oral epithelial cells are implicated in periodontal inflammation, we measured simvastatin effects on cytokine [interleukin (IL)-1β, IL-6, IL-8, IL-10, IL-12p70, and tumor necrosis factor α (TNFα)] production by cultured human epithelioid cell line KB cells in response to IL-1α. Simvastatin decreased production, an effect reversed by adding mevalonate or geranylgeranyl pyrophosphate (GGPP), but not farnesyl pyrophosphate (FPP). Simvastatin was found to reduce NF-κB and AP-1 promoter activity in KB cells. Our results support an anti-inflammatory effect of simvastatin on human oral epithelial cells.
収録刊行物
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- Inflammation and Regeneration
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Inflammation and Regeneration 27 (2), 107-111, 2007
一般社団法人 日本炎症・再生医学会
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詳細情報 詳細情報について
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- CRID
- 1390001205256734848
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- NII論文ID
- 10019482557
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- NII書誌ID
- AA11508953
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- COI
- 1:CAS:528:DC%2BD2sXlslWnurs%3D
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- ISSN
- 18808190
- 18809693
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- NDL書誌ID
- 8778669
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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