Eicosapentaenoic Acid Preserves Mitochondrial Quality and Attenuates Cardiac Remodeling After Myocardial Infarction in Rats
Eicosapentaenoic Acid Preserves Mitochondrial Quality and Attenuates Cardiac Remodeling After Myocardial Infarction in Rats
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DOI：
10.1007/s12265-023-10363-z
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发表时间：
2023-02-27
影响因子：
3.4
通讯作者：
Nakata，Tetsuo
中科院分区：
文献类型：
--
作者：
Kobara，Miyuki;Shiraishi，Tatsuya;Nakata，Tetsuo
二十碳五烯酸（EPA）降低缺血性心脏病的风险，是线粒体的一种成分。我们在此研究了膳食EPA是否介导了线粒体脂肪酸的组成、动力学和功能，从而导致心肌梗死（MI）后心脏重塑的减弱。结扎雄性大鼠的冠状动脉以诱导MI，然后用或不用EPA（1000 mg/kg/天）处理12周。心肌梗死后12周，EPA治疗改善了左心室收缩功能，并增加了非梗死区EPA的线粒体含量。ATP和线粒体复合物II，III和IV的活性的含量降低MI后，但保持EPA治疗与保存视神经萎缩1，线粒体融合蛋白。目前的结果表明，膳食EPA增加了线粒体EPA含量，并保留了线粒体融合蛋白的表达和能量代谢，从而减轻了MI后的左心室重塑。图形摘要
Eicosapentaenoic acid (EPA) reduces the risk of ischemic heart diseases and is a component of mitochondria. We herein investigated whether dietary EPA mediated mitochondrial fatty acid compositions, dynamics, and functions, resulting in the attenuation of cardiac remodeling after myocardial infarction (MI). The coronary artery of male rats was ligated to induce MI, and they were then treated with or without EPA (1000 mg/kg/day) for 12 weeks. The EPA treatment improved left ventricular systolic function and increased the mitochondrial content of EPA in the non-infarct region 12 weeks after MI. The content of ATP and mitochondrial complex II, III, and IV activities decreased after MI but were maintained by the EPA treatment in association with the preservation of optic atrophy 1, a mitochondrial fusion protein. The present results suggest that dietary EPA increased the mitochondrial content of EPA and preserved the expression of mitochondrial fusion proteins and energy metabolism, which attenuated left ventricular remodeling after MI.Graphical Abstract