中文摘要：

目的：采用体外炎症模型研究甘草总皂苷抗炎作用机制。方法：建立脂多糖（LPS）诱导巨噬细胞系RAW264.7细胞体外炎症模型,检测不同浓度甘草总皂苷对炎症因子生成与释放及花生四烯酸代谢通路中与前列腺素E2（PGE2）生成有关的关键酶的影响。结果：甘草总皂苷能显著降低LPS诱导的RAW264.7细胞一氧化氮（NO）、白细胞介素-1（IL-1）及肿瘤坏死因子-α（TNF-α）的释放,并通过抑制磷脂酶A2（PLA2）酶活性及环氧合酶-2（COX-2）表达而降低PGE2的合成。结论：甘草总皂苷抗炎作用与其减少巨噬细胞炎症介质生成与释放、抑制花生四烯酸代谢途径PGE2合成的关键酶密切相关。

英文摘要：

Objective： The inflammatory model in vitro was used to evaluate the anti-inflammatory mechanism of total saponins of Radix Glycyrrhiza. Method： RAW264. 7 macrophage line in mice was induced by LPS to set up the inflammatory model. To detect the effect of total saponins of Radix Glycyrrhiza on the release of inflammation factors and the key enzymes for arachidonic acid （AA） metabolism in synthesizing PGE2. Result： The total saponins of Radix Glycyrrhiza could significantly reduce the release of NO,IL-1 and TNF-α in LPS-induced RAW264. 7 macrophage line,and obviously decrease the synthesis of PGE2 by inhibiting PLA2 activity and the expression of COX-2. Conclusion： The anti-inflammatory mechanism of total saponins of Radix Glycyrrhiza may be related to reducing the release of inflammation factors in macrophage cell and inhibiting the key enzymes for AA metabolism pathway in synthesizing PGE2.