| Project/Area Number |
16K18884
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pharmacology in pharmacy
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Research Collaborator |
ISHIZAWA Yuki
URUSHIHARA Maki
Ehrenshaft Marilyn I.
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 腎虚血再灌流傷害 / フリーラジカル / immuno-spin trapping / 腎虚血再灌流障害 / 活性酸素種 / 内皮細胞 / ラジカル / ERK5 / 薬理学 |
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| Outline of Final Research Achievements |
To investigate the mechanisms of kidney ischemia-reperfusion injury (IRI) via reactive oxygen species (ROS) production, we used the immuno-spin trapping (IST) and endothelial cell-specific ERK5 deficient (ECKO) mice. Acute kidney injury was induced in the mice with a spin trapping agent, DMPO administration as well as in the mice without DMPO administration. By using IST, free radical production was found in the mouse kidney homogenate with hydrogen peroxide. We successfully created the ECKO mice. IRI induced angiotensinogen expression in the kidney medulla in the wild-type mice. ROS production, including free radical production, can be induced via local renin-angiotensin system activation in the kidney with IRI treatment.
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