目的 通过网络药理学和实验验证探讨白背叶楤木乙酸乙酯提取物对哮喘小鼠气道炎症的潜在作用机 制。方法 采用鸡卵白蛋白（OVA）诱导哮喘小鼠模型，评价白背叶楤木乙酸乙酯提取物对哮喘小鼠气道炎症的 改善作用；白背叶楤木乙酸乙酯提取物活性成分靶点与哮喘疾病靶点取交集后，构建“药物-成分-疾病-靶 点”的网络，进行 GO 与 KEGG 富集分析，对关键活性成分与通路核心靶点进行分子对接；对关键通路进行体 内验证。结果 白背叶楤木乙酸乙酯提取物显著改善哮喘小鼠肺组织气道炎症浸润、杯状细胞增生及气道高反 应；下调哮喘小鼠血清中 IgE 和 OVA-IgE 及肺泡灌洗液（BALF）中 IL-4、IL-5、IL-9、IL-13、IL-25、IL-33、 TSLP（P＜0.05，P＜0.01，P＜0.001）炎症因子的水平。网络药理学显示，白背叶楤木乙酸乙酯提取物干预哮喘 的 KEGG 分析富集于 MAPK、HIF-1、PI3K/Akt 等信号通路。分子对接结果显示，豆甾醇（stigmasterol）与 TLR4、MAPK8、MAPK14 有较强的结合。实验验证显示，白背叶楤木乙酸乙酯提取物降低了哮喘小鼠肺组 织 MYD88、p-P38/P-38 和 p-JNK/JNK 蛋白表达（P＜0.001，P＜0.01，P＜0.05）。结论 白背叶楤木乙酸乙酯 提取物可能是通过抑制 MAPK 通路的激活而发挥干预哮喘气道炎症作用。

Objective To explore the potential mechanism of ethyl acetate extract of Aralia chinensis var. nuda （EAEAC） in alleviating airway inflammation in asthmatic mice through network pharmacology and experimental validation. Methods An ovalbumin （OVA）-induced asthmatic mouse model was established to evaluate the ameliorative effects of EAEAC on airway inflammation. The intersection of EAEAC active component targets and asthma disease targets was used to construct a "drugs-components-diseases-targets" network. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analyses were performed， and molecular docking was conducted for key active components and core pathway targets. The key pathway was validated in vivo. Results EAEAC significantly improved airway inflammation infiltration，goblet cell hyperplasia，and airway hyperresponsiveness in the lung tissue of asthmatic mice. It down regulated the levels of IgE and OVA-IgE in serum and inflammatory cytokines （IL-4，IL-5，IL-9，IL-13，IL-25，IL-33，and TSLP） in bronchoalveolar lavage fluid （BALF）（P＜0.05，P＜ 0.01， P＜0.001）. Network pharmacology revealed that the KEGG analysis of EAEAC intervention in asthma was enriched in the MAPK，HIF-1，and PI3K/Akt signaling pathways. Molecular docking results showed that stigmasterol had strong binding affinities with TLR4，MAPK8，and MAPK14. Experimental validation demonstrated that EAEAC reduced the protein expression of MYD88，p-P38/P38，and p-JNK/JNK in the lung tissue of asthmatic mice （P＜ 0.001，P＜0.01，P＜0.05）. Conclusion EAEAC may exert its anti-asthmatic effects by inhibiting the activation of the MAPK pathway，thereby alleviating airway inflammation in asthma.

R285.5

国家自然科学基金项目（82260832，81860760）；云南省中医联合专项（202101AZ070001-159）；云南省“兴滇英才支持计划”（XDYCQNRC-2023-0529）；生物资源数字化开发应用（202002AA100007）；云南省南药可持续利用研究重点实验室项目（202105AG070012）。