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This study integrated network pharmacology with experimental validation to investigate these mechanisms. Network pharmacology identified 128 bioactive compounds and 135 potential targets of QXTMY, highlighting key anti\u2010AS targets such as TNF, IL6, insulin (INS), IL1B, MMP9, CCL2, and ALB, with the AGE\u2010RAGE signaling pathway as a central mechanism; principal active ingredients included quercetin, kaempferol, luteolin, and cryptotanshinone. In vitro experiments using THP\u20101\u2010derived macrophages induced with phorbol\u201012\u2010myristate\u201013\u2010acetate (PMA) and oxidized low\u2010density lipoprotein (ox\u2010LDL) showed that QXTMY significantly suppressed inflammatory responses, inhibited foam cell formation, and downregulated the AGE\u2010RAGE signaling pathway, as measured by Western blot, ELISA, cholesterol quantification, and Nile Red staining. These findings suggest that QXTMY may exert protective effects against AS, potentially via suppression of the AGE\u2010RAGE\u2010mediated inflammatory axis. 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