| Project/Area Number |
23390053
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General pharmacology
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| Research Institution | Chiba University |
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Principal Investigator |
NAKAYA HARUAKI 千葉大学, 医学(系)研究科(研究院), 教授 (60113594)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUMOTO Akio 千葉大学, 大学院・医学研究院, 准教授 (60437308)
NISHIDA Hirohumi 千葉大学, 大学院・医学研究院, 助教 (80513043)
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| Research Collaborator |
REIEN Yoshie 千葉大学, 医学部, 技術職員
MARUYAMA Hiroo 千葉大学, 医学部, 技術職員
TATIDANA Tomoko 千葉大学, 大学院・医学研究院, 派遣技術職員
SUZUKI Kazumasa 千葉大学, 大学院生
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| Project Period (FY) |
2011-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥20,020,000 (Direct Cost: ¥15,400,000、Indirect Cost: ¥4,620,000)
Fiscal Year 2013: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2012: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2011: ¥10,270,000 (Direct Cost: ¥7,900,000、Indirect Cost: ¥2,370,000)
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| Keywords | 活性酸素種 / 老化 / 心房細動 / アップストリームアプローチ / Mn-SOD欠損マウス / Mn-SODマウス |
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| Research Abstract |
Reactive oxygen species (ROS) are suggested to play an important role in the genesis of atrial fibrillation in elderly patients. However, a direct evidence of arrhythmogenic properties associated with chronic exposure to ROS is lacking. This study was undertaken to evaluate electrophysiological alterations induced by chronic exposure to ROS using heart/muscle-specific manganese-superoxide dismutase-deficient (H/M-SOD-/-) mice. Atrial action potential was prolonged with a decreased K+ current density and susceptibility to atrial fibrillation was increased. In atrial tissues of H/M-SOD-/- mice fibrotic changes and decreased expression of connexin 43 protein were observed. These electrophysiological and histological abnormalities were lessened by chronic intake of an antioxidant in H/M-SOD-/- mice. Thus, chronic exposure to ROS can increase susceptibility to atrial fibrillation and dietary intake of antioxidant nutrients may prevent oxidative stress-induced arrhythmias.
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