Project/Area Number |
25861153
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
General surgery
|
Research Institution | Mie University |
Principal Investigator |
Kuriyama Naohisa 三重大学, 医学(系)研究科(研究院), 講師 (80525329)
|
Research Collaborator |
FUJII Takehiro 三重大学, 医学(系)研究科(研究院)病態修復医学講座 肝胆膵・移植外科学, 助教
MATSUDA Akitoshi 三重大学, 医学(系)研究科(研究院)病態修復医学講座 肝胆膵・移植外科学, 医員
HIBI Tamami 三重大学, 医学(系)研究科(研究院)病態修復医学講座 肝胆膵・移植外科学, 実験助手
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 肝虚血再灌流障害 / 脂肪肝 / 抗炎症作用 / 虚血再灌流障害 / 活性化プロテインC / AMPK / ATP / 脾臓摘出 / marginal donor graft / 虚血再環流障害 |
Outline of Final Research Achievements |
We compared the cytoprotective effects of Activated protein C (APC) in non-steatotic and steatotic liver ischemia reperfusion injury (IRI). Methods: Mice were fed either normal diets (ND mice) or high fat diets (HF mice), were treated with APC or saline (control) and were performed IRI. In an in vitro study, primary steatotic hepatocytes were either untreated, or were treated with APC, then incubated with H2O2. Results: APC reduced serum transaminase levels and the inflammatory cells infiltration at 4 h in ND mice, while at 24 h in HF mice. APC inhibited sinusoidal endothelial injury in only ND mice. APC activated AMPK phosphorylation in only HF mice. In the in vitro study, APC increased AMPK phosphorylation, ATP concentration and survival rates of hepatocytes. Conclusion: In normal liver, APC attenuated initial damage by inhibiting inflammatory cell infiltration and sinusoidal endothelial injury. However, in steatotic liver, APC might attenuated late damage via activation of AMPK.
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