| Project/Area Number |
20591029
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Keio University |
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Principal Investigator |
SUZUKI Shigeaki Keio University, 医学部, 講師 (50276242)
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| Co-Investigator(Kenkyū-buntansha) |
TOMITA Yutaka 慶應義塾大学, 医学部, 講師 (60276251)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 臨床神経形態学 / 脳虚血 / Stat3 / AG-490 / サイトカイン / 脳梗塞 / 炎症反応 / 神経保護 / 脳循環 / leukemia inhibitory factor / リン酸化 |
|---|
| Research Abstract |
An increase in serum cytokine level has been reported in acute ischemic stroke patients by many investigators. Among the various molecules involved in the JAK-STAT pathway activated by cytokine, Stat3 is the most important and has attracted much attention. We have already proven that Stat3 phosphorylation is associated with neuroprotection against acute cerebral ischemia. The neuroprotective effects of Stat3 phosphorylation are also supported by other reports. We observed the rapid enhancement of Stat3 phosphorylation was detected after the injection of high-dose recombinant LIF into the cerebral cortex on the ischemic side in rat focal ischemia. We examined the possible treatment strategy using Stat3 phosphorylation over a longer period, such as the first 2-3 months after cerebral ischemia using selective pharmacological agents of this signaling. However, we failed to prove definitive effects of Stat3 phosphorylation in chronic cerebral ischemia. This reason may be explained that Stat3 protein can be activated by a variety of signals, including other growth factors, cytokines, and oxidative stress
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