我们应用网络药理学和分子对接分析来研究布鲁松宁E（BRE）治疗急性呼吸窘迫综合征（ARDS）的疗效，并确定BRE的核心成分、潜在靶点和作用机制。 SwissTargetprediction和SEA数据库用于预测BRE目标，GeneCards和OMIM数据库用于预测ARDS相关基因。将药物靶点和疾病靶点进行映射，获得交叉的药物靶点基因网络，然后将其上传到String数据库中进行蛋白质-蛋白质相互作用网络分析。交叉基因也上传到DAVID数据库进行基因本体富集分析和京都基因百科全书和基因组通路分析。进行分子对接分析以验证 BRE 与关键靶点的相互作用。最后，为了验证体内实验，我们建立了油酸诱导的ARDS大鼠模型，并通过组织学评估和酶联免疫吸附试验评估了BRE对ARDS的保护作用。总体而言，预测了BRE的79个目标和ARDS的3974个目标，交集后得到79个目标。 HSP90AA1、JUN、ESR1、MTOR 和 PIK3CA 等关键基因通过调节肿瘤坏死因子、核因子-κB 和 PI3K-Akt 信号通路在细胞核和细胞质中发挥重要作用。分子对接结果表明，BRE小分子可以自由结合到目标蛋白的活性位点。体内实验表明，BRE可以减轻ARDS相关的组织病理学变化、炎症因子的释放以及巨噬细胞的浸润和氧化应激反应。 BRE通过靶向、多途径发挥对ARDS的治疗作用。本研究还预测了BRE治疗ARDS的潜在机制，为深入、全面研究BRE治疗ARDS提供了理论基础。© 2023。作者，经德国Springer-Verlag GmbH独家授权，部分施普林格自然。

We applied network pharmacology and molecular docking analyses to study the efficacy of Broussonin E (BRE) in acute respiratory distress syndrome (ARDS) treatment and to determine the core components, potential targets, and mechanism of action of BRE. The SwissTargetprediction and SEA databases were used to predict BRE targets, and the GeneCards and OMIM databases were used to predict ARDS-related genes. The drug targets and disease targets were mapped to obtain an intersecting drug target gene network, which was then uploaded into the String database for protein-protein interaction network analysis. The intersecting gene was also uploaded into the DAVID database for gene ontology enrichment analysis and Kyoto encyclopedia of genes and genomes pathway analysis. Molecular docking analysis was performed to verify the interaction of BRE with the key targets. Finally, to validate the experiment in vivo, we established an oleic acid-induced ARDS rat model and evaluated the protective effect of BRE on ARDS by histological evaluation and enzyme-linked immunosorbent assay. Overall, 79 targets of BRE and 3974 targets of ARDS were predicted, and 79 targets were obtained after intersection. Key genes such as HSP90AA1, JUN, ESR1, MTOR, and PIK3CA play important roles in the nucleus and cytoplasm by regulating the tumor necrosis factor, nuclear factor-κB, and PI3K-Akt signaling pathways. Molecular docking results showed that small molecules of BRE could freely bind to the active site of the target proteins. In vivo experiments showed that BRE could reduce ARDS-related histopathological changes, release of inflammatory factors, and infiltration of macrophages and oxidative stress reaction. BRE exerts its therapeutic effect on ARDS through target and multiple pathways. This study also predicted the potential mechanism of BRE on ARDS, which provides the theoretical basis for in-depth and comprehensive studies of BRE treatment on ARDS.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.