BACKGROUNDBreast cancer (BC) is a prevalent malignancy among women with strong heterogeneity. This study is designed to investigate the therapeutic effects of Huanglian Jiedu Tang (HLJDT) on BC progression and reveal its potential mechanism.METHODSThe effects of different concentrates of HLJDT on the viability, proliferation, migration, and invasion of BC cells were measured by CCK-8 assay, EdU staining, scratch test, and transwell assay, respectively. The levels of inflammatory factors and oxidative stress indicators were detected by ELISA. RhoA/ROCK pathway related protein was measured by western blot. A xenograft tumor model was constructed to explore the effects of HLJDT in vivo. Hematoxylin eosin staining was exploited to observe the pathological changes. Tumor proliferation was detected by immunohistochemistry (Ki67). Macrophage markers were detected by flow cytometry and RT-PCR. Furthermore, the ROCK agonist was used for feedback functional experiments.RESULTSThere was a concentration-dependent increase in the inhibitory impact of HLJDT on the viability, proliferation, migration, and invasion of BC cells (MCF-7 and MDA-MB-23). Moreover, HLJDT inhibit inflammation (TNF-α, IL-6 and IL-1β), oxidative stress (ROS, MDA and GSH) and RhoA/ROCK pathway. HLJDT regulated inflammatory microenvironment in BC, with increased IL-10, IL-4 levels and reduced TGF-β. In vivo, HLJDT restrained the tumor growth and proliferation, diminishing inflammatory infiltration and reducing malignancy. Additionally, HLJDT significantly increased F4/80 +CD86 and iNOS levels, as well as the decreased F4/80 +CD163 + and Arg1 levels. The treatment of ROCK agonist weakened the inhibitory effects of HLJDT on inflammation and BC progression.CONCLUSIONHLJDT may regulate inflammatory microenvironment to suppress BC progression through inhibiting the RhoA/ROCK pathway.