Astragaloside IV (AST-IV) is a major active ingredient of astragalus, with a neuroprotective effect. The current study is aimed to investigate the impact of AST-IV on the M1/M2 microglial activation in response to lipopolysaccharide (LPS) stimulation, how AST-IV attenuated microglia-mediated neuronal damage, and the molecular mechanisms underlying AST-IV's protection of neurons against microglia-mediated neuronal damage. Our results showed that AST-IV partially protected microglia from death evoked by LPS and downregulated the release of pro-inflammatory (M1) mediators including interleukin (IL)-1β, IL-6, tumour necrosis factor α (TNF-α) and nitric oxide, as well as the expression of Toll-like receptors 4 (TLR4), MyD88, and nuclear factor κB (NF-κB) of these cells. In contrast, AST-IV elevated the production of anti-inflammatory cytokine IL-10 and expression of arginase 1, an M2 marker of microglia, whose conditioned medium promoted PC12 neurons survival. These results indicate that AST-IV exerts an anti-inflammatory effect on microglia, possibly through inhibiting TLR4/NF-κB signalling pathways, and protects neurons from microglia-mediated cell death through conversion of microglia from inflammatory M1 to an anti-inflammatory M2 phenotype.

中文翻译：

---

黄芪甲苷IV通过促进小胶质细胞极化保护神经元免受小胶质细胞介导的细胞损伤。

黄芪甲苷IV（AST-IV）是黄芪的主要活性成分，具有神经保护作用。当前的研究旨在研究AST-IV对脂多糖（LPS）刺激响应中M1 / M2小胶质细胞活化的影响，AST-IV如何减轻小胶质细胞介导的神经元损伤以及AST-IV保护神经胶质的分子机制。神经元对抗小胶质细胞介导的神经元损害。我们的结果表明，AST-IV可部分保护小胶质细胞免受LPS引起的死亡，并下调促炎性（M1）介质的释放，包括白介素（IL）-1β，IL-6，肿瘤坏死因子α（TNF-α）和硝酸以及这些细胞的Toll样受体4（TLR4），MyD88和核因子κB（NF-κB）的表达。相反，AST-IV可提高抗炎细胞因子IL-10的产生和精氨酸酶1（小胶质细胞的M2标记）的表达，其条件培养基可促进PC12神经元的存活。这些结果表明，AST-IV可能通过抑制TLR4 /NF-κB信号传导途径对小胶质细胞产生抗炎作用，并通过将小胶质细胞从炎症M1转变为抗炎M2表型，保护神经元免受小胶质细胞介导的细胞死亡。 。