心肌纤维化（MF）是许多心血管疾病的先进病理表现，可引起心力衰竭和恶性心律失常。然而，目前治疗MF缺乏特定药物。Ginsenoside Re在大鼠中具有抗MF作用，但其机制仍不清楚。因此，我们通过构建小鼠急性心肌梗死（AMI）模型和AngⅡ诱导的心脏成纤维细胞（CFs）模型来研究Ginsenoside Re的抗MF作用。用miR-489的模拟和抑制器转染CFs，研究miR-489的抗MF作用。在AMI小鼠模型和AngⅡ诱导的CFs模型中，通过超声波、ELISA、组织病理学染色、Transwell测试、免疫荧光、Western blot和qPCR研究了Ginsenoside Re对MF及其相关机制的作用。miR-489降低了正常CFs和AngⅡ处理的CFs中α-SMA，胶原Ⅰ，胶原Ⅲ和myd88的表达，并抑制了NF-κB p65的磷酸化。Ginsenoside Re可以改善心功能，抑制胶原沉积和CFs迁移，促进miR-489的转录，并降低myd88的表达和NF-κB p65的磷酸化。miR-489可以有效抑制MF的病理过程，并且其机制至少部分与myd88 / NF-κB途径的调节有关。Ginsenoside Re可以改善AMI和AngⅡ诱导的MF，其机制至少部分与miR-489 / myd88 / NF-κB信号通路的调节有关。因此，miR-489可能是抗MF的潜在靶点，Ginsenoside Re可能是MF治疗的有效药物。©2021 韩国人参学会。Elsevier B.V.出版服务。

Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and AngⅡ induced cardiac fibroblasts (CFs) model.The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the AngⅡ-induced CFs model.MiR-489 decreased the expression of α-SMA, collagenⅠ, collagen Ⅲ and myd88, and inhibited the phosphorylation of NF-κB p65 in normal CFs and CFs treated with AngⅡ. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-κB p65.MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-κB pathway. Ginsenoside Re can ameliorate AMI and AngⅡ induced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-κB signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF.© 2021 The Korean Society of Ginseng. Publishing services by Elsevier B.V.