The Impact of Xi Huang Wan on the Expression Levels of Myeloid-derived Suppressor Cells and Tumor Necrosis Factor-alpha/Nuclear Factor Kappa B Signaling Pathway in Mice Bearing Breast Cancer

Abstract Objective: To investigate the effects of Xi Huang Wan on the expression of myeloid-derived suppressor cells (MDSCs) and the activity of the tumor necrosis factor-alpha (TNF-α)/nuclear factor kappa B (NF-κB) signaling pathway in mice with breast cancer. Materials and Methods: This study comprised six experimental groups: a blank control group, a model control group, three treatment groups receiving low, medium, and high doses, respectively, and a group treated with capecitabine tablets. Flow cytometry was employed to quantify the levels of MDSCs and their subsets. Serum concentrations of inflammatory cytokines were measured by enzyme-linked immunosorbent assay. Tissue expression of inflammatory mediators was evaluated using immunohistochemistry. The mRNA and protein expression levels of the TNF-α/NF-κB signaling pathways were assessed using real-time polymerase chain reaction and Western blotting, respectively. Results: The model group exhibited the highest levels of MDSCs overall. In contrast, the Xi Huang Wan treatment groups showed a reduction in total MDSCs. The granulocytic MDSCs were most elevated in the model group, whereas monocytic MDSCs were least expressed. No statistically significant differences in granulocytic or monocytic MDSC levels were observed between any Xi Huang Wan dosage groups and the model group. Compared with the model group, Xi Huang Wan treatment significantly reduced the expression levels of TNF-α, interleukin-6 (IL-6), and interferon-gamma in peripheral blood. Immunohistochemical analysis indicated minimal TNF-α protein expression and elevated IL-6 expression in the model group, showing opposing trends. The mRNA and protein expression levels of TNF-α and NF-κB p65 were highest in the model group but markedly reduced across all Xi Huang Wan dosage groups. Conclusions: Xi Huang Wan has the potential to inhibit the growth of transplanted tumors. In addition, it could modulate MDSC levels, regulate the expression of associated inflammatory factors, and alter the mRNA and protein expression linked to the TNF-α/NF-κB signaling pathway.