Protective effect for antioxidative peptide against disruption of blood brain barrier induced ischemic injury
Project/Area Number |
24500423
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Nerve anatomy/Neuropathology
|
Research Institution | Juntendo University |
Principal Investigator |
URABE Takao 順天堂大学, 医学部, 教授 (60291663)
|
Co-Investigator(Kenkyū-buntansha) |
SIMISAWA Tatsuo 東京大学, 医学部, 講師 (90231365)
|
Research Collaborator |
MIYAMOTO Nobukazu
TANAKA Yasutaka
|
Project Period (FY) |
2012-04-01 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | アドレノメデュリン / 抗酸化ペプチド / 虚血性大脳白質障害 / 酸化ストレス / 高血糖 / 加齢 / 脳保護 / 認知障害 / 脳虚血 / 白質障害 / 血管内皮細胞 / 血液脳関門 / 細胞内シグナル伝達 |
Outline of Final Research Achievements |
This study demonstrated that ischemic white matter injury was increased in adrenomedullin (AM) deficiency, which induced oxidative stress. We indicated that adrenomedullin downregulation results in increase in oxidative stress after cerebral hypoperfusion in mice cerebral white matter. Oxidative stress was detected in oligodendrocytes, with a larger increase in the AM deficiency group. The number of oligodendrocyte progenitor cells gradually increased after prolonged hypoperfusion, whereas oligodendrocytes decreased following a transient increase, but the ratio of increase was mild in the AM deficiency group. White matter injury was more exacerbated because of hyperglycemia in aged AM deficiency group. The results indicated that adrenomedullin may be an important target in the control of ischemic white matter injury.
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Report
(4 results)
Research Products
(29 results)