| Project/Area Number |
16K15320
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied pharmacology
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
小田切 優樹 崇城大学, 薬学部, 教授 (80120145)
丸山 徹 熊本大学, 薬学部, 教授 (90423657)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | alfa1-acid glycoprotein / kidney disease / TLR4 / macrophage / 腎線維化 / ビタミンD / AGP / α1-酸性糖蛋白質 / アドリアマイシン腎障害 / マクロファージ / 糸球体バリア / α1-酸性糖タンパク質 / 慢性腎臓病 |
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| Outline of Final Research Achievements |
Human alfa1-acid glycoprotein (AGP) is known as an acute phase reactant, and we have recently found anti-inflammatory effects of AGP. In this study, the effect of AGP on renal protection on adriamycin-nephropathy (AN) mice was investigated. As a result, administration of AGP to AN mice reduced proteinuria and improved kidney tissue inury. At that time, the expression level of TNF-alfa and macrophage marker F4/80 in the kidney was decreased. Addition of AGP to macrophages resulted in an increase in IL-10 production and a decrease in iNOS expression. At the same time, gene expression of CD 163 also increased. In conclusion, we discovered for the first time that AGP exerts a renoprotective effect through the calming of the inflammatory response caused by macrophages.
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