目的 筛选金岗清瘟颗粒抗炎活性成分并测定其含量。方法 采用二甲苯致小鼠耳肿胀急性炎症模型和脂多糖（lipopolysaccharide，LPS）诱导小鼠单核巨噬细胞RAW264.7炎症模型，分别以小鼠耳肿胀度以及炎症因子一氧化氮（nitric oxide，NO）、白细胞介素-6（interleukin-6，IL-6）和肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）为指标，评价金岗清瘟颗粒的抗炎作用。通过网络药理学预测金岗清瘟颗粒具有抗炎作用的化学成分和潜在靶点，对作用靶点进行基因本体（gene ontology，GO）功能和京都基因与基因组百科全书（Kyoto encyclopedia of genes and genomes，KEGG）通路富集分析，对化学成分的吸收、分布、代谢、排泄、毒性（absorption，distribution，metabolism，excretion，toxicity，ADMET）性质进行筛选作为有效成分，再通过高效液相色谱（HPLC）法测定有效成分含量。结果 在动物实验中，与模型组相比，金岗清瘟颗粒可以显著减轻小鼠耳肿胀的炎症反应（P<0.01）。在细胞实验中，与对照组相比，模型组细胞上清液中NO、IL-6和TNF-α水平明显升高（P<0.01）；与模型组相比，金岗清瘟颗粒含药血清组细胞上清液中炎症因子水平显著降低（P<0.01）。网络药理学分析结果显示，筛选得到43个化学成分，619个成分靶点和584个疾病靶点，作用靶点128个，主要富集在炎症反应、一氧化氮生物合成过程的正调控等556条生物过程，以及缺氧诱导因子-1（hypoxia inducible factor-1，HIF-1）信号通路、TNF信号通路等108条通路。结合ADMET性质筛选得到齐墩果酸、熊果酸、咖啡酸和连翘苷作为有效成分，其质量分数分别为0.65、0.68、0.59、2.38 mg/g。结论 体内外实验证实金岗清瘟颗粒具有抗炎作用，其作用机制可能是通过作用于前列腺素G/H合酶2（prostaglandin G/H synthase 2，PTGS2）、IL-6、TNF等靶点调控HIF-1信号通路、TNF信号通路等信号通路。齐墩果酸、熊果酸、咖啡酸和连翘苷是金岗清瘟颗粒的抗炎活性成分，可作为制剂的质量控制指标。

Objective To screen and determine the anti-inflammatory active components of Jinggang Qingwen Granules (金岗清瘟颗粒, JGQW). Methods Acute inflammation model of xylene induced ear swelling in mice and lipopolysaccharide (LPS) induced inflammation model of RAW264.7 cells were used to evaluate the anti-inflammatory effects of JGQW, using the degree of ear swelling in mice and inflammatory factors nitric oxide (NO), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) as indicators. The chemical components and potential targets of JGQW with anti-inflammatory effects were predicted by network pharmacology. The targets were analyzed by gene ontology (GO) function and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis. Absorption, distribution, metabolism, excretion, toxicity (ADMET) and other properties of chemical components were screened to obtain effective components. Finally, content of active components was determined by high performance liquid chromatography (HPLC). Results In animal experiments, JGQW significantly reduced the inflammatory response of ear swelling in mice compared with model group (P < 0.01). In cell experiments, levels of NO, IL-6 and TNF-α in supernatant produced by cells in model group were significantly higher than control group (P < 0.01), while the levels of inflammatory factors in JGQW-containing serum group were significantly lower than model group (P < 0.01). Network pharmacological analysis obtained 43 chemical components, 619 component targets, 584 disease targets and 128 action targets, which were mainly concentrated in 556 biological processes such as inflammatory response and positive regulation of nitric oxide biosynthesis, as well as 108 pathways such as hypoxia inducible factor-1 (HIF-1) signal pathway and TNF signal pathway. Combined with ADMET screening, oleanolic acid, ursolic acid, caffeic acid and forsythin were obtained as target component with the contents of 0.65, 0.68, 0.59 and 2.38 mg/g, respectively. Conclusion In vitro and in vivo experiments confirmed that JGQW has anti-inflammatory effects, and its mechanism may be related to the interaction with prostaglandin G/H synthase 2 (PTGS2), IL-6, TNF and other targets to regulate HIF-1 signaling pathway, TNF signaling pathway and other signaling pathways. Oleanolic acid, ursolic acid, caffeic acid and forsythin are anti-inflammatory active ingredients of JGQW and can be used as quality control indicators for the formulation.

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中国科学院科技服务网络计划（STS计划）区域重点项目（KFJ-STS-QYZD-2021-03-002）；广西自然科学基金资助项目（2020GXNSFAA238035）；广西科技基地和人才专项（桂科AD20238058）