Project/Area Number |
13470283
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cerebral neurosurgery
|
Research Institution | Gunma University |
Principal Investigator |
SAITO Nobuhito Gunma University, Department of Neurosurgery, Professor, 医学部, 教授 (60262002)
|
Co-Investigator(Kenkyū-buntansha) |
TAKAHASHI Akio Gunma University, Department of Neurosurgery, Assistant Professor, 医学部, 講師 (60261856)
TOSAKA Masahiko Gunma University, Department of Neurosurgery, staff, 医学部, 助手 (40323357)
豊田 富勝 東京大学, 医学部, 助手 (00251257)
|
Project Period (FY) |
2001 – 2003
|
Project Status |
Completed (Fiscal Year 2003)
|
Budget Amount *help |
¥12,300,000 (Direct Cost: ¥12,300,000)
Fiscal Year 2003: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2002: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2001: ¥6,900,000 (Direct Cost: ¥6,900,000)
|
Keywords | cerebral ischemia / MAP kinase / signal transduction / 免疫抑制剤 |
Research Abstract |
MEK is in the course of MAP kinase cascade and bears the signal transduction of growth factors and protects cells from various insults. However, it is reported recently that inhibition of MEK activity may protect neurons from excitotoxic insults. In this study, we aimed to clarify weather MEK mediates death signal or not. Constitutively active MEK1 was adenoviral transdused in primary cultured neurons. Four days after MEK1 adenovirus infection, neuronal death was evaluated by LDH measurement of the supernatant. MEK1 induced neuronal death dose-dependently. A MEK inhibitor, U0126, prevented the death. Thus, MEK1 was considered to mediate death signal in the cultured neurons. To examine the effect of MEK inhibitor in vivo, focal cerebral ischemia by middle cerebral artery occlusion was induced in rats after administration of U0126 or vehicles. In our experiment, U0126 did not have protective effect against cerebral ischemia. Further investigation is indicated to clarify the difference.
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