Project/Area Number |
23592648
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Plastic surgery
|
Research Institution | Kobe University |
Principal Investigator |
USAMI Makoto 神戸大学, 保健学研究科, 教授 (00193855)
|
Co-Investigator(Kenkyū-buntansha) |
TERASHI Hiroto 神戸大学, 医学部附属病院形成外科, 教授 (80217421)
|
Co-Investigator(Renkei-kenkyūsha) |
ISHIKAWA Michiko (AOYAMA Michiko) 神戸大学, 保健学研究科, 保健学研究員 (40566121)
MAESHIGE Noriaki 神戸大学, 保健学研究科, 助教 (90617838)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | 創傷治癒学 / 短鎖脂肪酸 / ω-3系多価不飽和脂肪酸 / ケロイド / 線維芽細胞 / 細胞・組織 / 脂質 / 線維化 |
Research Abstract |
We revealed the antifibrogenic effects of short chain fatty acids and polyunsaturated fatty acids, and the best combination is butyrate and docosahexaenoic acid among those fatty acids. As the mechanisms, we found the inhibitory effects on the expressions of profibrotic factors including alpha-SMA, TGF-beta1, type I collagen and type III collagen, and the inhibition of cell proliferation, and promotion of apoptosis in normal human dermal and keloid fibroblasts. These antifibrogenic effects were also found in the pathological models with addition of proinflammatory cytokines or pseudomonas aeruginosa derived LPS or TGF-beta1 stimulation. As the key mechanisms of these effects, the production of PGE2, as an antifibrogenic lipid mediator, and the histone acetylation by butyrate were revealed.
|