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通过构建的细菌脂多糖(LPS)诱导小鼠巨噬细胞(RAW264.7)的体外炎症模型,研究了不同质量浓度人参皂苷Rh2硫酸化衍生物B2(Rh2-B2)对TNF-α、IL-6、IL-1β和IL-10合成的影响,以及对NF-κB信号通路的影响。结果显示,1mg/L和5mg/L的人参皂苷Rh2-B2能显著抑制RAW264.7合成TNF-α、IL-6和IL-1β(P<0.01),同时显著促进IL-10的合成(P<0.01),并且通过显著抑制IκBα的降解而阻止NF-κB/p65易位入核(P<0.01)。结果表明,人参皂苷Rh2-B2可能通过阻断NF-κB信号通路,抑制LPS诱导的炎性细胞因子的产生,进而发挥其抗炎作用。
The in vitro inflammatory model of murine macrophage (RAW264.7) was induced by bacterial lipopolysaccharide (LPS), and the effect of Rh2-B2, a derivative of ginsenoside Rh2 on TNF-αand IL- 6, IL-1β and IL-10 synthesis, as well as the impact of NF-κB signaling pathway. The results showed that 1mg / L and 5mg / L of ginsenoside Rh2-B2 significantly inhibited the synthesis of TNF-α, IL-6 and IL-1β by RAW264.7 (P <0.01) <0.01), and prevented the translocation of NF-κB / p65 into the nucleus by significantly inhibiting the degradation of IκBα (P <0.01). The results showed that ginsenoside Rh2-B2 could inhibit the production of inflammatory cytokines induced by LPS by blocking the NF-κB signaling pathway and thus exert its anti-inflammatory effect.