基于细菌脂多糖（Lipopolysaccharide，LPS）诱导的RAW264.7细胞炎症模型，该文深入研究了人参皂苷Rg2的抗炎效果，并利用聚合酶链式反应（Polymerase Chain Reaction，PCR）、实时荧光定量PCR（Real-Time Quantitative polymerase Chain Reaction，RT-qPCR）、蛋白印迹等技术检测分析了人参皂苷Rg2对LPS诱导RAW264.7细胞炎症相关基因和蛋白的表达水平。结果显示，人参皂苷Rg2呈剂量依赖性抑制炎症细胞一氧化氮（Nitric Oxide，NO）的释放（P<0.05）以及一氧化氮合酶（Inducible Nitric Oxide Sythase，iNOS）、环氧化酶2（Cyclooxygenase-2,COX2）、肿瘤坏死因子α（Tumor Necrosis Factor-α，TNF-α）和白细胞介素1β（Interleukin-1β，IL-1β）等炎症相关基因的转录水平（P<0.05）。扫描电镜（Scanning Electron Microscope，SEM）观察分析显示人参皂苷Rg2可以有效改善LPS诱导的RAW264.7细胞形态。蛋白印迹结果显示人参皂苷Rg2能够抑制PI3K、PDK1、AKT、GSK-3β等蛋白的磷酸化和NF-κB 蛋白入核。该研究结果表明人参皂苷Rg2具有明确的抗炎作用，能够通过PI3K/AKT/NF-κB信号通路减轻LPS诱导的RAW264.7细胞炎症。该研究结果有助于全面理解人参皂苷Rg2的抗炎活性及其机制，为相关功能食品开发奠定基础。

The anti-inflammatory effects of ginsenoside Rg2 were investigated based on a bacterial lipopolysaccharide (LPS)-induced inflammation model of RAW264.7 cells. The expression levels of inflammation-related genes and proteins in the model were analyzed using PCR, RT-qPCR, and western blotting. The results demonstrated that ginsenoside Rg2 dosedependently inhibited the release of nitric oxide from inflammatory cells (P<0.05) and transcription levels of inflammationrelated genes, including inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α, and interleukin-1β (P<0.05). Scanning electron microscopy analysis showed that ginsenoside Rg2 improved the morphology of inflammatory RAW264.7 cells after LPS induction. Western blotting results revealed that ginsenoside Rg2 inhibited the phosphorylation of PI3K, PDK1, AKT, and GSK-3β and prevented NF-κB from entering the nucleus. These results suggest that ginsenoside Rg2 has an anti-inflammatory effect and can reduce LPS-induced inflammation of RAW264.7 cells via the PI3K/AKT/NF-κB signaling pathway. The findings of this study improve the understanding of the anti-inflammatory activity of ginsenoside Rg2 and associated mechanism and provide a foundation for the development of related functional foods.

江苏省高等学校基础科学（自然科学）研究重大项目（23KJA550001）