最近，一些研究表明，心肌缺血再灌注（I/R）损伤与肠道菌群有关。然而，研究显示异源棕榈素（irisin）对心肌I/R损伤具有益处，因此引起了对其作用机制的兴趣。因此，本研究调查了irisin是否干预心肌I/R损伤期间的肠道菌群和肠黏膜屏障。研究发现，irisin能够减少炎症细胞的浸润和心肌组织的破裂、降低心肌酶水平、减少心肌梗死（MI）面积。此外，数据显示，irisin逆转了I/R诱导的肠道菌群失调，表现为放线菌门（Actinobacteriota）丰度的降低和厚壁菌门（Firmicutes）丰度的增加，并保持肠道屏障完整性，减少代谢性内毒素血症，并抑制前炎症细胞因子白细胞介素1β（IL-1β）、白细胞介素6（IL-6）和肿瘤坏死因子α（TNF-α）的产生。根据结果，irisin可能成为缓解心肌I/R损伤及相关疾病的理想候选药物，通过缓解肠道菌群失调、内皮功能障碍和抗炎特性。版权所有：© 2023 Liu等。该文是一篇以实验为基础的研究，采用创作共用许可证，允许在任何媒介中进行无限制使用、传播和复制，只要保持原始作者和出处的署名。

Recently, myocardial ischemia-reperfusion (I/R) injury was suggested associated with intestinal flora. However, irisin has demonstrated beneficial effects on myocardial I/R injury, thus increasing interest in exploring its mechanism. Therefore, whether irisin interferes in gut microbiota and gut mucosal barrier during myocardial I/R injury was investigated in the present study. Irisin was found to reduce the infiltration of inflammatory cells and fracture in myocardial tissue, myocardial enzyme levels, and the myocardial infarction (MI) area. In addition, the data showed that irisin reverses I/R-induced gut dysbiosis as indicated by the decreased abundance of Actinobacteriota and the increased abundance of Firmicutes, and maintains intestinal barrier integrity, reduces metabolic endotoxemia, and inhibits the production of proinflammatory cytokines interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α). Based on the results, irisin could be a good candidate for ameliorating myocardial I/R injury and associated diseases by alleviating gut dysbiosis, endothelial dysfunction and anti-inflammatory properties.Copyright: © 2023 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.