| Project/Area Number |
23659279
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Applied pharmacology
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SAKAI Satoshi 筑波大学, 医学医療系, 講師 (30282362)
SHIMANO Hitoshi 筑波大学, 医学医療系, 教授 (20251241)
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| Co-Investigator(Renkei-kenkyūsha) |
MARUYAMA Hidekazu 筑波大学, 附属病院, 病院講師 (30528493)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 心不全 / 慢性炎症 / 酸化ストレス / 不全心筋 / 炎症反応 |
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| Research Abstract |
The activation of angiotensin system contributes to the development of failing heart. Chronic administration of angiotensin II (AngII) lowered cardiac ejection faraction (EF) in wild mice, however, it did not change in mice deficient of the transcription factor SREBP-1. Reactive oxygen species is involved in AngII-induced organ injury. The expression level of both the master regulator for antioxidant Nrf2, a transcription factor, and Nrf2 regulating gene for antioxidative stress was significantly decreased by AngII administration in the heart; conversely, the expression level of them did not differ in KO. Taken together, cardiac dysfunction induced by Ang II may be associated with the reduced expression of Nrf2 and its regulatory gene against antioxidative stress.
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