Effect ofAlhagi honey polysaccharide on immunosuppressive activity by regulating Toll-like receptor 4
This study elucidates the regulatory mechanism of Alhagi honey polysaccharide on Toll-like receptor 4(TLR4).An immunosuppressive mouse model was established using C57BL/6J mice,and a RAW 264.7 model induced by TAK-242 in-hibitor was constructed.In the mouse model,Alhagi honey polysaccharide were administered at 800 mg/kg,while the RAW 264.7 model received interventions with different concentrations of Alhagi honey polysaccharide(25,50,75,100 μg/mL).Enzyme-linked immunosorbent assay(ELISA)was employed to measure cytokine levels in mouse serum and RAW 264.7 cell culture supernatant.Protein immunoblotting and real-time quantitative PCR(qRT-PCR)were conducted to detect the ex-pression of TLR4,myeloid differentiation factor 88(MyD88),and tumor necrosis factor-α receptor associated factor 6(TRAF6)in relevant tissues and cells.Results indicate that Alhagi honey polysaccharide significantly increased the spleen index,thymus index,and serum levels of interleukin-2(IL-2),interleukin-4(IL-4),tumor necrosis factor-α(TNF-α),im-munoglobulin G(IgG),and immunoglobulin M(IgM)in immunosuppressive mice.In the TAK-242 inhibitor-induced cell model,Alhagi honey polysaccharide increased the secretion of interleukin-1β(IL-1β),interleukin-6(IL-6),interleukin-12(IL-12),TNF-α,and nuclear factor-κB(NF-κB).Furthermore,Alhagi honey polysaccharide reversed the downregulation of TLR4 and MyD88/TRAF6 expression.Alhagi honey polysaccharide can activate the immune response of TLR4 receptors by modulating the MyD88 pathway.
Alhagi honey polysaccharideToll-like receptor 4macrophage RAW 264.7immunosuppression
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维普
