| Project/Area Number |
17K11063
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Anesthesiology
|
|---|
| Research Institution | Jikei University School of Medicine |
|---|
Principal Investigator |
Kohei Ikeda 東京慈恵会医科大学, 医学部, 講師 (60792471)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
三尾 寧 東京慈恵会医科大学, 医学部, 教授 (00266686)
山田 勇磨 北海道大学, 薬学研究院, 准教授 (60451431)
|
|---|
| Project Period (FY) |
2017-04-01 – 2021-03-31
|
| Project Status |
Completed (Fiscal Year 2020)
|
| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | 心停止蘇生 / 虚血再灌流傷害 / ミトコンドリア / Drug Delivery System |
|---|
| Outline of Final Research Achievements |
Mitochondrial dysfunction following ischemia/reperfusion injury including cardiac arrest and CPR is characterized by an impairment of mitochondrial function which leads to pro-apoptotic signaling and cell death. No pharmacological agent has yet been found to improve clinical outcomes after cardiac arest. We developed a new mitochondria targeted nano-particle involving active form vitamin B1, VB1-MITO-Porter. This VB1-MITO-Porter statistically increased ATP turn over of SHSY5Y cell's mitochondria in-vitro. However, VB1-MITO-Porter did not improve 10-day survival and histological brain injury on murine cardiac arrest model.
|
| Academic Significance and Societal Importance of the Research Achievements |
心停止後の脳障害の治療薬の開発は喫緊の課題である。本研究ではミトコンドリアでのATP合成能を有意に上昇させる活性型ビタミンB1ナノ粒子の作製に成功したが、生体（マウス）における蘇生後生存率と脳障害における治療効果を認めることはできなかった。
|
