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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 are important immune cells in the central nervous system and are also the main effector cells in the inflammatory response. Paeoniflorin proved to be able to effectively inhibit the inflammatory response, has great medicinal value in the regulation of immunity. The purpose of this article is to elucidate the inhibitory effect of paeoniflorin on the inflammation and phagocytosis of BV2 cells in inflammatory reaction and explore the underlying mechanism. In vitro experiments, lipopolysaccharide (LPS) was used to induce the inflammatory response in BV2 cells. Paeoniflorin could effectively inhibit the production of TNF-α and NO and the phagocytosis of BV2 cells in BV2 cells. Moreover, IL-10-STAT3 The signal pathway was activated. The inhibitory effect of paeoniflorin was significantly reduced after using STAT3 inhibitor JSI-124, the expression of TNF-α and NO increased, and phagocytosis of BV2 cells increased. The above results show that paeoniflorin can effectively inhibit BV2 cell inflammation and phagocytosis, the process dependent on IL-10-STAT3 signaling pathway activation. This will deepen our understanding of the mechanism of paeoniflorin inhibiting microglial inflammation.