Asparagus Polysaccharide Ameliorates TNF-α-Mediated MH7A Cell Dysfunction and Collagen-Induced Arthritis in Mice

Although Rheumatoid arthritis (RA) management has improved substantially with modern pharmacological therapies, many patients still fail to achieve sustained treatment targets. This study investigated the therapeutic effects and potential mechanisms of asparagus polysaccharide (APS) in tumor necrosis factor-α (TNF-α)-induced MH7A cell dysfunction and collagen-induced arthritis (CIA) in mice. In vitro, MH7A cells were treated with different concentrations of APS, and cell viability, apoptosis, cell cycle distribution, and related protein and gene expression were assessed. In vivo, CIA model was established in mice, followed by APS administration. Paw volume, joint histopathology, serum cytokine levels, and the splenic Th17 cell proportion were evaluated. APS (≥ 3 mg/mL, 48 h) decreased MH7A cell viability. APS (3, 4, 5 mg/mL, 24 h) promoted apoptosis and inhibited proliferation in TNF-α-treated MH7A cells. APS (5 mg/mL, 24 h) downregulated Bcl-2 and cell cycle-related genes and suppressed NF-κB pathway activation. In the CIA mouse model, APS reduced paw volume, alleviated joint inflammation and tissue damage, decreased serum TNF-α, interleukin-6 (IL-6), IL-17A levels, increased IL-10 levels, and inhibited splenic Th17 cell expansion in a dose-dependent manner, without a significant effect on Treg cell proportion. APS exerts anti-arthritic effects in vitro and in vivo by regulating synoviocyte proliferation and apoptosis, inflammatory cytokine balance, and Th17 cell differentiation. The in vitro mechanism was associated with inhibition of NF-κB signaling. These findings provide preliminary experimental evidence supporting further investigation of APS as a candidate therapeutic agent for RA.