芍药苷通过IL-10-STAT3信号通路抑制脂多糖诱导BV2细胞炎症与吞噬作用

Paeoniflorin Inhibits Lipopolysaccharide-induced Microglia Inflammation and Phagocytosis through IL-10-STAT3 Signaling Pathway

小胶质细胞是中枢神经系统中重要免疫细胞,也是炎症反应中的主要效应细胞。芍药苷被证实能有效抑制炎症反应,在调节免疫方面具有巨大药用价值。本文旨在阐明BV2细胞炎症反应中芍药苷对细胞炎症及吞噬的抑制作用,并探索其中潜在机制。体外实验利用脂多糖(lipopolysaccharide,LPS)诱导BV2细胞发生炎症反应,芍药苷能有效抑制BV2细胞TNF-α和NO的产生以及BV2细胞异常增加的吞噬功能,并且在此过程中IL-10-STAT3信号通路被激活;芍药苷的抑制作用在我们使用STAT3抑制剂JSI-124后显著降低,TNF-α和NO的表达量增加、BV2细胞的吞噬功能增强。上述结果表明,芍药苷能有效抑制BV2细胞炎症作用及吞噬作用,这一过程中依赖IL-10-STAT3信号通路的激活。这将加深我们对芍药苷抑制小胶质细胞炎症作用机制的认识。

Microglia is an important immune cell in the central nervous system, and also is a major effector cell in the process of inflammation. Numerous studies have shown that paeoniflorin （PF） , which has anti-inflammatory effects in immunity, has great medical value. This study aims to investigate the potential mechanisms involved in the inhibitory effects of PF on inflammation and phagocytosis during microglia inflammation. During the inflammation induced by lipopolysaccharide （LPS） , PF effectively inhibited the production of TNF-α and NO, and attenuated the phagocytosis of microglia BV2 cells. During this process, the IL-10-STAT3 signaling pathway was activated. After the treatment of JSI-124, an inhibitor of STAT3, the anti-inflammation effects of PF vanished, whereas the production of TNF-tx and NO and the rate of microglia phagocytosis was increased. These results suggested that PF could efficiently inhibit the microglia inflammation and phagoeytosis, which was dependent on the activation of IL-10-STAT3 signaling pathway. These findings mechanism of PF in microglia. may improve our understanding of the anti-inflammation