| Project/Area Number |
12670650
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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 |
Circulatory organs internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
OHNO Minoru Faculty of Medicin, The University of Tokyo, Lecturer, 医学部・附属病院, 講師 (00185349)
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| Co-Investigator(Kenkyū-buntansha) |
TSUKAMOTO Kazuhisa Faculty of Medicin, The University of Tokyo, Assistant, 医学部・附属病院, 助手 (20251233)
ISHIZAKA Nobukazu Faculty of Medicin, The University of Tokyo, Assistant, 医学部・附属病院, 助手 (20270879)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | heme oxygenase / Oxidative stress / CO / heart / bilirubin / Ferrtine / ヘムオキシゲナーゼ / 心筋 / 鉄 / 遺伝子治療 / 炎症 / 移植 / 再灌流 |
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| Research Abstract |
Enhanced production of reactive oxygen species plays a role in myocardial injury following ischemia/reperfusion. Heme oxygenase-1 (HO-1) is a hemecatabolizing enzyme that is induced by and acts against oxidant-induced tissue injury. HO-1 expression increased as early as 24 h after reperfusion, Strong HO-1 expression was seen in monocytes/ macrophages and myofibroblaste. Next, we examined whether the induction of HO-1 could ameliorate cardiac injury following ischemia/reperfusion Intraperitoneal hemin injection for 2 days prior to the operation resulted in an about 2.8-fold increase in HO-1 expression in the rat heart. Hemin treatment significantly decreased infarct area compared to the control, which was reversed by the coadministration of an HO inhibitor in a dosedependent manner. Our data suggest that induction of HO-1 can reduce the cardiac injury in vivo following ischemia/reperfusion.
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