| Project/Area Number |
24659586
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | Nagoya University |
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Principal Investigator |
KOMORI KIMIHIRO 名古屋大学, 医学(系)研究科(研究院), 教授 (40225587)
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| Co-Investigator(Kenkyū-buntansha) |
NARITA Hiroshi 名古屋大学, 医学部附属病院, 助教 (00528739)
KODAMA Akio 名古屋大学, 医学部附属病院, 病院助教 (10528748)
SUGIMOTO Masayuki 名古屋大学, 医学部附属病院, 病院助教 (00447814)
坂野 比呂志 名古屋大学, 医学部附属病院, 助教 (80584721)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 血管外科学 / 末梢動脈閉塞症 / 静脈グラフト血管内膜肥厚 / 重症虚血肢 / 動脈瘤 |
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| Research Abstract |
(Background) We investigated whether metformin modulates the revascularization processes in vivo employing a hindlimb model of ischemia-induced angiogenesis. (Methods)Wild-type (WT) mice or eNOS deficient (eNOS-KO) mice were randomly divided into two groups. Mice were treated with or without metformine and were subjected to unilateral hind limb ischemia.(Results)WT mice (metformin group) showed accelerated limb perfusion following hindlimb ischemic surgery based upon laser Doppler measurements of blood flow and increased capillary density in ischemic muscle compared to non-treated mice. Metformin group significantly enhanced ischemia-induced increase in AMPK and eNOS phosphorylation levels in WT mice. In eNOS-KO mice, metformin significantly increased the phosphorylation of AMPK in ischemic tissue, but did not affect blood flow recovery in ischemic limb. (Conclusions)Metformin could promote revascularization in response to tissue ischemia via an AMPK/eNOS-dependent mechanism.
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