Inflammation and oxidative stress are becoming more recognized as risk factors for ischemic stroke. Paeoniflorigenone (PA) has diverse pharmacological effects that include anti-inflammatory and antioxidant properties. However, the specific mechanisms by which PA affects cerebral ischemic stroke have not been studied. Our objective was to investigate the potential targets and mechanisms of PA in preventing cerebral ischemic stroke. We obtained the potential targets of PA from the SwissTargetPrediction, Super-PRED, and SEA Search Server databases. The GSE97537 dataset was utilized to identify gene targets related to ischemic stroke. The overlapping targets were imported into the STRING database to construct a protein–protein interaction network, and enrichment analyses were conducted using R software. Rats were pretreated with PA for three weeks before undergoing MCAO and reperfusion. H&E staining, ELISA, and qRT-PCR analyses were then performed to explore the potential mechanisms of PA. In the study, we identified 439 potential targets for PA and 1206 potential targets for ischemic stroke. Out of these, there were 71 common targets, which were found to be primarily associated with pathways related to oxidative stress and inflammation. The results from animal experiments showed that PA was able to improve nerve function and reduce inflammatory cytokines and oxidative stress in the MCAO-induced ischemic stroke model. Additionally, the expression of core genes in the MCAO + HPA group was significantly lower compared to the MCAO group. Our study revealed that the potential mechanisms by which PA prevents ischemic stroke involve oxidative stress and inflammation. These findings provide important theoretical guidance for the clinical use of PA in preventing and managing ischemic stroke.

炎症和氧化应激越来越被认为是缺血性中风的危险因素。芍药烯酮 (PA) 具有多种药理作用，包括抗炎和抗氧化特性。然而，PA影响脑缺血性卒中的具体机制尚未研究。我们的目的是研究 PA 预防脑缺血性卒中的潜在靶点和机制。我们从 SwissTargetPrediction、Super-PRED 和 SEA Search Server 数据库中获得了 PA 的潜在目标。GSE97537 数据集用于识别与缺血性中风相关的基因靶标。将重叠的靶标导入STRING数据库构建蛋白质-蛋白质相互作用网络，并使用R软件进行富集分析。在进行 MCAO 和再灌注之前，对大鼠进行 PA 预处理三周。然后进行 H&E 染色、ELISA 和 qRT-PCR 分析，以探索 PA 的潜在机制。在这项研究中，我们确定了 439 个 PA 潜在靶点和 1206 个缺血性中风潜在靶点。其中，有 71 个共同目标，被发现主要与氧化应激和炎症相关途径相关。动物实验结果表明，PA能够改善MCAO诱发的缺血性中风模型的神经功能，减少炎症细胞因子和氧化应激。此外，MCAO+HPA组的核心基因表达量显着低于MCAO组。我们的研究表明，PA 预防缺血性中风的潜在机制涉及氧化应激和炎症。这些发现为PA预防和治疗缺血性脑卒中的临床应用提供了重要的理论指导。