Kobara Miyuki, Shiraishi Tatsuya, Noda Kazuki, Toba Hiroe, Nakata Tetsuo
Department of Clinical Pharmacology, Division of Pathological Science, Kyoto Pharmaceutical University, 5 Misasagi Nakauchi-cho, Yamashina-ku, Kyoto, 607-8414, Japan.
J Cardiovasc Transl Res. 2023 Aug;16(4):816-827. doi: 10.1007/s12265-023-10363-z. Epub 2023 Feb 27.
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.
二十碳五烯酸（EPA）可降低缺血性心脏病的风险，并且是线粒体的组成成分。我们在此研究了膳食中的EPA是否介导了线粒体脂肪酸组成、动态变化及功能，从而减轻心肌梗死（MI）后的心脏重塑。结扎雄性大鼠冠状动脉以诱导MI，然后对其进行为期12周的EPA（1000毫克/千克/天）治疗或不治疗。EPA治疗改善了左心室收缩功能，并在MI后12周增加了非梗死区域线粒体中EPA的含量。MI后ATP含量以及线粒体复合物II、III和IV的活性降低，但EPA治疗可维持这些指标，并与线粒体融合蛋白视神经萎缩蛋白1的保留相关。目前的结果表明，膳食中的EPA增加了线粒体中EPA的含量，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。
