| Project/Area Number |
23590117
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Biological pharmacy
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| Research Institution | Nihon University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
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| Keywords | 脳虚血 / 再灌流障害 / GR103691 / ROS / HT22細胞 / 低酸素再酸素化細胞死 / 酸化ストレス / 細胞死 |
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| Research Abstract |
It is estimated that there are 1,500,000 patients with cerebrovascular disease (CVD) and that cerebral ischemia (stroke) is responsible for more than 60% of CVD in Japan. Recent data also shows that the mortality rate due to CVD is decreasing, however number of patients do not decrease, and therapeutic options is still limited. Reactive oxygen species and other free ragicals generated during cerebral ischemia/reperfusion are critical mediators of neuronal cell damage. Edaravone, a radical scavenger, has been shown to be effective for stroke patients and is clinically used in Japan. However, adoption of edaravone is limited because of side effects, such as renal toxicity.
Aim to develop of new therapeutic agents for ischemia/reperfusion injury, new cerebroprotective agents were explored in newly synthetic GR103691 derivatives. The most important results in this study is finding of some useful compounds for the injury and these compounds were more effective than edaravone.
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