| Project/Area Number |
21591835
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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 |
Cerebral neurosurgery
|
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| Research Institution | University of Yamanashi |
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Principal Investigator |
KINOUCHI Hiroyuki 山梨大学, 大学院・医学工学総合研究部, 教授 (30241623)
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|---|
| Co-Investigator(Kenkyū-buntansha) |
SUGITA Masao 山梨大学, 医学部附属病院, 講師 (70235886)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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|---|
| Keywords | PPARγ / 脳虚血 / アポトーシス / Akt |
|---|
| Research Abstract |
Synthetic peroxisome proliferator-activated receptorγ(PPARγ) ligands, thiazolidinediones, are used for the treatment of type 2diabetes. In addition, they have pleiotropic effects such as neuroprotective effects against ischemic neuronal injury ; however, the mechanism of neuroprotective effects is still obscure. In this study, we examined the expression of PPARγafter transient forebrain ischemia, and assessed the neuroprotective effects of thiazolidinediones in this model. We also studied the effects of thiazolidinediones on Akt/GSK-3βand STAT3, key pathways of prosurvival signaling after ischemia. We revealed that PPARγis upregulated mainly in neurons after ischemia, and thiazolidinediones have a neuroprotective effects against ischemic neuronal injury via activation of Akt/GSK-3βand STAT3pathways.
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