【摘要】 目的 探讨周建伟教授利用中风协方Ⅱ号治疗中风后遗症的作用机制，借助网络药理学与分子对接技术，从分子水平揭示其“多成分-多靶点-多通路”协同调控特征。方法 通过TCMSP数据库筛选中风协方Ⅱ号活性成分及潜在靶点，靶点经Uniprot标准化处理。疾病相关靶点来源于GeneCards、OMIM，交集靶点导入STRING数据库构建蛋白质-蛋白质互作（PPI）网络，利用Cytoscape、R 4.4.3分析筛选核心靶点。利用DAVID平台对交集靶点进行GO功能注释与KEGG通路富集分析。选取主要成分与核心靶点，通过PubChem数据库获取结构数据，采用AutoDock Vina进行分子对接分析。结果 中风协方Ⅱ号共筛得226个活性成分、245个潜在靶点，与中风后遗症交集靶点126个。槲皮素、木犀草素、山奈酚为核心成分，TP53、STAT3、TNF、IL1B、MAPK1等为关键靶点。GO分析显示靶点主要参与氧化应激、炎症反应等生物过程；KEGG富集通路包括脂质与动脉粥样硬化通路、IL-17信号通路、TNF信号通路、NF-κB信号通路等。分子对接表明槲皮素与FOS、木犀草素与MAPK1结合能分别为-2.49kcal/mol、-2.10kcal/mol，结合效果稳定。结论 中风协方Ⅱ号可能通过TP53、STAT3、TNF、IL1B、MAPK1等靶点及脂质与动脉粥样硬化、IL-17、TNF等通路干预中风后遗症的关键病理环节，为其临床应用和机制研究提供理论依据。更多还原

【Abstract】 Objective To investigate the mechanism of stroke Xiefang Ⅱ(SXⅡ) in the treatment of sequelae of stroke based on Professor Zhou Jianwei’s clinical experience, using network pharmacology and molecular docking to reveal its multi-component, multi-target, and multi-pathway synergistic regulatory characteristics at the molecular level. Methods Active ingredients and potential targets of SXⅡ were retrieved from the TCMSP database, with target names standardized via Uniprot. Disease-related targets were collected from GeneCards and OMIM. Common targets were imported into the STRING database to construct a protein-protein interaction(PPI) network. Core targets were identified using Cytoscape and R 4.4.3. Functional enrichment analysis of Gene Ontology(GO) terms and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathways was performed using the DAVID platform. Key active components and core targets were selected for molecular docking analysis using AutoDock Vina, with structures obtained from PubChem. Results A total of 226 active ingredients and 245 potential targets of SX Ⅱ were identified, with 126 overlapping targets related to sequelae of stroke. Key components included quercetin, luteolin, and kaempferol; central targets were TP53, STAT3, TNF, IL1B, and MAPK1. GO analysis indicated involvement in biological processes such as oxidative stress and inflammatory response. KEGG pathways included lipid and atherosclerosis, IL-17 signaling pathway, TNF signaling pathway, and NF-kappa B signaling pathway. Molecular docking demonstrated strong binding stability, with quercetin-FOS and luteolin-MAPK1 binding energies of-2.49 kcal/mol and-2.10 kcal/mol, respectively. Conclusion SXⅡ may intervene in the key pathological links of Sequelae of cerebral infarction through targets such as TP53, STAT3, TNF, IL1B, MAPK1, and pathways involving lipids and atherosclerosis, IL-17, TNF, etc., providing a theoretical basis for its clinical application and mechanism research.更多还原