Qianjinba is derived from the dried root of a legume vine and is known for its plant polysaccharide, which has demonstrated anti-inflammatory, analgesic, and neuroprotective properties. Despite these known effects, its immunomodulatory potential remains underexplored. This study aimed to investigate the immunoregulatory effects of Qianjinba polysaccharide (QJBDT) in a murine model of rheumatoid arthritis (RA) and elucidate its mechanism of action in inhibiting the disease. To assess the immunomodulatory effects, RAW264.7 macrophage cells were stimulated with bacterial lipopolysaccharide (LPS) and subsequently treated with varying concentrations of QJBDT or total glucoside of paeonic acid (TGP). Cell proliferation and the expression levels of mitogen-activated protein kinase p38 and nuclear factor NF-κB proteins were evaluated. Following the successful modeling of RA in mice, different doses of QJBDT and TGP were administered via intragastric administration once daily for 21 d. Mice were divided into normal, model, QJBDT low-, medium-, and high-dose groups, along with a positive control group (TGP group), each comprising 10 mice. Organ coefficients were calculated, immune indexes in blood cells were determined, and alterations in T helper cell 17 (Th17) and regulatory T cells (Treg) were analyzed using flow cytometry. Compared to the normal group, cell proliferation rates significantly increased across all groups (P < 0.05). Elevated expressions of p38 and NF-κB proteins were observed in the model group, QJBDT low- and medium-dose groups (P < 0.05). Various systemic immune inflammation indexes, including systemic immune inflammation index (SII), total inflammation systemic index (AISI), and systemic inflammation response index (SIRI), platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR)，monocyte-to-lymphocyte ratio (MLR), showed increments (P < 0.05). Additionally, body weight and organ coefficients of the thymus, spleen, and liver decreased in both the model and low-dose groups (P < 0.05). Moreover, Th17 levels increased while Treg levels decreased across all groups (P < 0.05), resulting in a heightened Th17 to Treg ratio in the model and low-dose groups (P < 0.05). Notably, the QJBDT medium-dose, high-dose, and positive control groups demonstrated significant inhibitory effects on cell proliferation compared to the model group (P < 0.05), along with reduced expression levels of p38 and NF-κB (P < 0.05). Furthermore, various immune indicators from routine blood tests exhibited different degrees of decrease (P < 0.05), while immune indices displayed increases (P < 0.05). The low-, medium-, and high-dose groups of QJBDT, as well as the positive control group, showed decreased Th17 levels, elevated Treg levels, and diminished Th17 to Treg ratios (P < 0.05). Additionally, there was no statistically significant difference in efficacy between the QJBDT high-dose and TGP groups (P > 0.05). In conclusion, this study demonstrated that QJBDT exerted potent immunomodulatory effects on RA in mice in a dose-dependent manner. Its mechanism of action might involve the inhibition of NF-κB activation by suppressing the p38 MAPK signaling pathway.
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