This study aimed to delineate the mechanism by which GSW modulates inflammation-linked insulin signaling in a PCOS-relevant granulosa cell model under metabolic stress, with a focus on the TNF-α/PI3K/Akt axis.<h4>Methods</h4>Network pharmacology based on serum-absorbed constituents identified by UPLC-MS/MS was integrated with <i>in vitro</i> validation using dexamethasone- and insulin-challenged human KGN cells to model selected PCOS-relevant cellular phenotypes. The gene discussed is AKT1; the disease is polycystic ovary syndrome.