| Project/Area Number |
20791613
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Periodontal dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
FUJITA Tsuyoshi Hiroshima University, 病院, 助教 (80379883)
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| Project Period (FY) |
2008 – 2009
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| Project Status |
Completed (Fiscal Year 2009)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 歯周病予防 / 歯肉上皮細胞 / マレイン酸イルソグラジン / ケモカイン / 細胞接着因子 / イルソグラジンマレイン酸 / Aggregatibacter actinomycetemcomitans / CINC-2α / E-cadherin / CXCL-1 / IL-8 / p44 / 42 Map kinase (ERK) / tight junction / adherence junction / 歯周病予防薬 |
|---|
| Research Abstract |
By regulating the intercellular junctional complex and chemokine secretion in human gingival epithelial cells (HGEC), irsogladine maleate (IM) may be useful to prevent periodontal disease. To clarify the effects and regulatory mechanism of IM in vivo and in vitro, we examined the expression of E-cadherin and neutrophil chemotaxis induced by A. actinomycetemcomitans under IM pretreatment. In the present study, we demonstrated that IM inhibited the A. actinomycetemcomitans-induced inflammatory response in gingival epithelium by suppressing neutrophil migration in vivo and in vitro. In addition, IM recovered the A. actinomycetemcomitans-induced reduction in E-cadherin, suggesting enhancement of the barrier function of gingival epithelium. In conclusion, IM may control A. actinomycetemcomitans-induced gingival inflammation by regulating neutrophil migration and E-cadherin expression in gingival epithelium.
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