神经炎症是中枢神经系统损伤后的表现，微胶质细胞的M1/M2极化与神经炎症的发展密切相关。本研究利用多个数据库收集关于芹菜素和微胶质细胞极化的靶标。在获得共同靶标后，构建了蛋白质相互作用（PPI）网络，并进行进一步分析以获得核心网络。通过基因富集分析，分子对接核心网络与芹菜素之间的关系，通过体外实验检测微胶质细胞的极化程度及相关靶标蛋白的表达情况。共获得了77个共同的靶标，进一步分析得到的核心网络包含了38个蛋白质。GO和KEGG分析结果显示，芹菜素对炎症反应调控、白细胞介素（IL）-17和肿瘤坏死因子（TNF）信号通路具有影响。通过体外实验，我们证实芹菜素的使用可以降低诱导型一氧化氮合酶（iNOS）、IL-6、TNF-α、p-NFκBIA（p-IκB-α）、p-NFκB p65和MMP9的表达，同时上调Arg-1和IL-10的表达。本研究揭示了芹菜素诱导微胶质细胞M2极化抑制神经炎症反应的多种潜在机制。© 2023. Springer Nature Limited.

Neuroinflammation manifests following injury to the central nervous system (CNS) and M1/M2 polarization of microglia is closely associated with the development of this neuroinflammation. In this study, multiple databases were used to collect targets regarding luteolin and microglia polarization. After obtaining a common target, a protein-protein interaction (PPI) network was created and further analysis was performed to obtain the core network. Molecular docking of the core network with luteolin after gene enrichment analysis. In vitro experiments were used to examine the polarization of microglia and the expression of related target proteins. A total of 77 common targets were obtained, and the core network obtained by further analysis contained 38 proteins. GO and KEGG analyses revealed that luteolin affects microglia polarization in regulation of inflammatory response as well as the interleukin (IL)-17 and tumor necrosis factor (TNF) signaling pathways. Through in vitro experiments, we confirmed that the use of luteolin reduced the expression of inducible nitric oxide synthase (iNOS), IL-6, TNF-α, p-NFκBIA (p-IκB-α), p-NFκB p65, and MMP9, while upregulating the expression of Arg-1 and IL-10. This study reveals various potential mechanisms by which luteolin induces M2 polarization in microglia to inhibit the neuroinflammatory response.© 2023. Springer Nature Limited.