Mechanism of anti-inflammatory property of dietary fiber through glucan receptor on small intestinal epitherial cells
Project/Area Number |
24500974
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Eating habits, studies on eating habits
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Research Institution | Kobe University |
Principal Investigator |
MIZUNO Masashi 神戸大学, (連合)農学研究科(研究院), 教授 (00212233)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | Lentinan / Dectin-1 / 多糖類 / 抗炎症作用 / レンチナン / 炎症生腸疾患 / βグルカン / 腫瘍壊死因子受容体 / 小腸上皮細胞 / 樹状細胞 / 炎症性腸疾患 / インターロイキン8 |
Outline of Final Research Achievements |
In this study, the mechanism of anti-inflammation by lentinan was investigated. Lentinan was orally administered to Dectin-1 knockout (Dectin-1 KO) mice which were treated by DSS to induce colitis. Oral administration of lentinan (100 μg/mouse/day) did not show any significant improvement in DSS-induced Dectin-1 KO mice. Moreover, TNFR1 mRNA expression in intestinal epithelial cells was decreased by lentinan administration to wild type mice, but not Dectin-1 KO mice. These results revealed that lentinan may exert its anti-inflammatory activities through the beta-glucan receptor Dectin-1 with the decrease of TNFR1 in intestinal epithelial cells.
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Report
(4 results)
Research Products
(13 results)