New approach for the diabetic nephropathy using the inhibition by GSK3
Project/Area Number |
21591034
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Kidney internal medicine
|
Research Institution | Kumamoto University |
Principal Investigator |
NAKAYAMA Yushi 熊本大学, 医学部附属病院, 講師 (00363531)
|
Co-Investigator(Kenkyū-buntansha) |
TOMITA Kimio 熊本大学, 大学院・生命科学研究部, 教授 (40114772)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 糖尿病 / 糖尿病性腎症 / GSK-3β / BIO / TGF-β1 / バルプロ酸 / STZ / NRK-52E cells |
Research Abstract |
Diabetes mellitus was induced by STZ administration to the SD rat. The 2 Z, 3 E-6-bromoindirubin-3-oxime(BIO), a GSK-3 s inhibitor, was administrated peritoneally. In diabetic rat the urinary protein excretion was reduced by BIO administration. The TGF-s1 mRNA expression of glomeruli was suppressed by BIO treatment. It was suggested that the suppression of TGF-s1 by BIO could be involved the amelioration of diabetic nephropathy.
|
Report
(4 results)
Research Products
(23 results)