Acute myocardial infarction (AMI) is an acute heart disease. Cycloastragenol, as a natural product, inhibits inflammation and protects cardiomyocytes. Cycloastragenol (Y006) modulates inflammation in AMI is not known. To explore the function of Cycloastragenol in AMI, this study investigated the effect of Y006 and its mechanisms both in vitro and in vivo. Y006 influences the concentration of 11 proteins, as shown by a proteomics analysis, immunohistochemistry and western blotting. Among these 11 proteins, Erk1/2, PLCG1, IKBKG, and ZEB1 are related to inflammatory regulation. BAX, COX2, and GSK3β are involved in modulating cardiomyocyte apoptosis, and RhoA and DSC2 are directly associated with myocardial function. However, the functions of ARHGAP17 and Rit2 in heart are less well established. Additionally, Y006 suppressed TNF-α, IFN-γ and IL-17 production in PBMCs (peripheral blood monocytes) from patients with acute myocardial infarction and enhanced IL-10 and IL-4 expression. Similar results were obtained in a rat model of AMI by flow cytometry detection and ELISA. Our findings indicate that Y006 protects rats from AMI through direct or indirect inhibition of inflammation and cardiomyocyte apoptosis. However, the specific mechanism of Y006's protective function requires further study. Nonetheless, this research revealed a novel aspect for the treatment of myocardial infarction. SIGNIFICANCE: In the present study, we undertook the first proteomic evaluation of Cycloastragenol (Y006) function in acute myocardial infarction (AMI). Y006 significantly improved myocardial function in vivo by regulating multiple molecular expressions. Hypoxia is a direct reason for AMI. And our data support a role of Y006 in gene expression, cell apoptosis under hypoxia. The conclusions of this research assist to explain the potential molecular mechanism in Cycloastragenol treating AMI and supply a new method for ameliorating AMI.

中文翻译：

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应用定量蛋白质组学方法鉴定急性心肌梗死大鼠中环黄芪醇介导的与心脏保护相关的差异表达蛋白。

急性心肌梗塞（AMI）是一种急性心脏病。天然的环雌三醇可以抑制炎症并保护心肌细胞。环雌三醇（Y006）可以调节AMI中的炎症。为了探讨环雌三醇在AMI中的功能，本研究调查了Y006的作用及其体内外机制。如蛋白质组学分析，免疫组织化学和蛋白质印迹所示，Y006影响11种蛋白质的浓度。在这11种蛋白质中，Erk1 / 2，PLCG1，IKBKG和ZEB1与炎症调节有关。BAX，COX2和GSK3β参与调节心肌细胞凋亡，RhoA和DSC2与心肌功能直接相关。但是，ARHGAP17和Rit2在心脏中的功能尚不完善。此外，Y006抑制TNF-α，急性心肌梗死并增强IL-10和IL-4表达的患者PBMC（外周血单核细胞）中的IFN-γ和IL-17产生。通过流式细胞术检测和ELISA在AMI大鼠模型中获得了相似的结果。我们的发现表明，Y006通过直接或间接抑制炎症和心肌细胞凋亡来保护大鼠免于AMI。但是，Y006保护功能的具体机制有待进一步研究。然而，这项研究揭示了治疗心肌梗塞的新方面。重大意义：在本研究中，我们进行了Cycloastragenol（Y006）在急性心肌梗死（AMI）中的功能的首次蛋白质组学评估。Y006通过调节多种分子表达显着改善了体内的心肌功能。低氧是AMI的直接原因。并且我们的数据支持在缺氧条件下Y006在基因表达和细胞凋亡中的作用。这项研究的结论有助于解释环己三醇治疗AMI的潜在分子机制，并为改善AMI提供了一种新方法。