作为人参的主要生物活性物质，多数人参皂苷已被证实具有良好的抗炎作用，但是其抗炎机制研究较少，尤其是人参皂苷F2。因此，该研究基于脂多糖（Lipopolysaccharide，LPS）刺激RAW264.7细胞产生炎症，构建体外细胞炎症模型，探究人参皂苷F2的抗炎作用。细胞活力实验表明人参皂苷F2在100 μmol/L内对细胞无毒性作用，为安全浓度范围。人参皂苷F2可以显著抑制LPS刺激RAW264.7细胞NO释放，且呈剂量依赖性抑制（0~100 μmol/L）。人参皂苷F2（50、100 μmol/L）也呈剂量依赖性抑制一氧化氮合酶（iNOS）和肿瘤坏死因子（TNF-α）的mRNA表达，100 μmol/L时显著抑制iNOS和TNF-α的mRNA表达。经人参皂苷F2处理可显著下调iNOS蛋白表达，但对COX2蛋白表达无显著促进作用（P>0.05）。此外，经扫描电镜（SEM）观察，100 μmol/L人参皂苷F2处理可以显著改善LPS刺激RAW264.7细胞的细胞形态改变。蛋白印迹表明，人参皂苷F2提高了PDK1、AKT、IκB-α蛋白的表达，降低了AKT蛋白磷酸化、NF-κB的核易位。该文研究结果表明人参皂苷F2具有较好的抗炎作用，并可能通过AKT/IκB-α/NF-κB信号通路发挥其抗炎作用，可为相关天然抗炎药物的开发提供理论支撑。

Most ginsenosides (the main bioactive substances in ginseng) have been shown to exert potent anti- inflammatory effects, but their anti-inflammatory mechanisms, especially that of ginsenoside F2 (GF2), are incompletely understood. This study was conducted to explore the anti-inflammatory effect of GF2 in an in vitro model of inflammation using LPS-induced RAW264.7 cells. Cell viability analysis revealed that the safe concentration threshold of GF2 to be 100 μmol/L. GF2 significantly inhibited NO release in a dose-dependent manner (0~100 μmol/L) in LPS-induced RAW264.7 cells. GF2 (50, 100 μmol/L) also inhibited the mRNA expression of iNOS, IL-1β, COX2, and TNF-α. GF2 markedly downregulated the protein expression of iNOS, but not that of COX2. Further, treatment with 100 μmol/L GF2 markedly attenuated LPS-induced cell morphology changes in RAW264.7 cells. A western blot showed that GF2 increased PDK1, AKT, and IκB-α protein expression, and decreased AKT phosphorylationand NF-κB nuclear translocation. Our findings demonstrate that GF2 exerts potent anti-inflammatory effects and suggest that these effects are achieved through the AKT/IκB-α/NF-κB signaling pathway. This study can thus provide theoretical support for the development of natural anti-inflammatory drugs.

江苏省区域环境与现代农业协同创新中心（HSXT30411）；江苏省大学生创新创业训练计划项目（202210323091Y）