The effect of interleukin-11 in a donation after circulatory death heart model

Research Project

Project/Area Number	26462082
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Cardiovascular surgery
Research Institution	Chiba University
Principal Investigator	KOUNO Hiroki 千葉大学, 医学部附属病院, 助教 (40375803)
Co-Investigator(Kenkyū-buntansha)	松宮護郎千葉大学, 大学院医学研究院, 教授 (20314312) 石田敬一千葉大学, 大学院医学研究院, 特任准教授 (40375671) 藤尾慈大阪大学, 薬学研究科, 教授 (20359839)
Project Period (FY)	2014-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000) Fiscal Year 2016: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000) Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Keywords	IL-11 / 心筋保護効果 / サイトカイン療法 / 心臓血管外科
Outline of Final Research Achievements	<Objective> The effect of IL-11 on warm ischemia was examined using a rat Langendorff heart model. <Method> Rats were allocated into IL-11-treated and untreated groups. Both groups were subjected to 25 min of warm ischemia followed by 60 min of reperfusion. The functional recovery of the reperfused heart was compared. Coronary effluents were collected to measure myocardial biomarkers. Myocardial necrosis and apoptosis were quantified using electron microscopy and staining techniques. <Results> The IL-11 group showed better contractile performance indicating improved recovery. The biomarkers were not significantly different. Electron microscopy revealed partial necrosis in both groups, but apoptosis was not present in either group. <Conclusion> IL-11 treatment improved the contractile performance of the heart subjected warm ischemia. This may be due to the alleviation of necrosis caused by IL-11, but another mechanism eliciting the cytokine's cytoprotective function may exist.