目的 阐明金菱子散治疗胆汁反流性胃炎（BRG）的化学成分和药理机制。通过口服该模型溶液建立大鼠BRG模型。口服金LZP，连续35 d。测定胃残留率以及血清中肿瘤坏死因子（TNF）-α、白细胞介素（IL）-6、胃泌素的水平，并收集胃组织进行组织病理学分析。我们使用超高效液相色谱结合 Q Exactive Focus 质谱来鉴定 JLZP 中的化学成分。然后，构建蛋白质-蛋白质相互作用和草药-化合物-靶标网络来筛选潜在的生物活性化合物和靶标。然后进行京都基因和基因组百科全书通路分析，以阐明 JLZP 介导的 BRG 治疗所涉及的通路。构建核心化合物-靶点-通路相互作用网络后，进行分子对接，研究核心生物活性化合物与两个候选靶点[RAC-α丝氨酸/苏氨酸蛋白激酶（AKT1）和磷脂酰肌醇4,5-二磷酸的结合自由能3-激酶催化亚基α亚型（PIK3CA）]。JLZP提取物显着促进胃排空，调节细胞因子（TNF-α和IL-6）的释放，改善胃泌素分泌和粘膜修复。 JLZP 中初步表征了 56 种化合物。此外，网络药理学和分子对接结果表明，生物碱和黄酮类化合物可能是金LZP治疗BRG的生物活性化合物。 JLZP 可能通过调节磷脂酰肌醇-4,5-二磷酸 3-激酶蛋白激酶 B、缺氧诱导因子-1、丝裂原激活蛋白激酶、叉头盒 O、TNF 和 IL-17 信号通路来改善 BRG 进展期间的粘膜修复.我们阐明了金LZP治疗BRG的化学成分和药理机制，为临床应用提供依据。

To elucidate the chemical profile and the pharmacological mechanism by which Jinlingzi powder (, JLZP) treats bile reflux gastritis (BRG).A BRG model was established in rats by oral administration of the model solution. JLZP was orally administered for 35 d. Residual gastric rate and tumor necrosis factor (TNF)-α, interleukin (IL)-6, and gastrin levels in the serum were measured, and stomach tissues were collected for histopathological analysis. We used ultra-high performance liquid chromatography coupled with Q Exactive Focus mass spectrometry to identify the chemical ingredients in JLZP. Then, protein-protein interaction and herb-compound-target networks were constructed to screen potential bioactive compounds and targets. Kyoto Encyclopedia of Genes and Genomes pathway analysis was then performed to elucidate the pathway involved in the JLZP-mediated treatment of BRG. After constructing the core compound-target-pathway interaction network, molecular docking was performed to study the binding free energy of core bioactive compounds and two candidate targets [RAC-alpha serine/threonine-protein kinase (AKT1) and phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform (PIK3CA)].JLZP extracts significantly promoted gastric emptying, regulating the release of cytokines (TNF-α and IL-6) and improving gastrin secretion and mucosal repair. Fifty-six compounds were tentatively characterized in JLZP. Moreover, the network pharmacology and molecular docking results showed that alkaloids and flavonoids might be the bioactive compounds in JLZP that treat BRG. JLZP might improve mucosal repair during BRG progression by modulating the phosphatidylinositol-4,5-bisphosphate 3-kinase-protein kinase B, hypoxia inducible factor-1, mitogen-activated protein kinase, forkhead box O, TNF, and IL-17 signaling pathways.We elucidated the chemical constituents and the pharmacological mechanism of JLZP in treating BRG and provided a basis for clinical application.