Microglia cells are the main mediators of neuroinflammation. Activation of microglia often aggravates the pathological process of various neurological diseases. Natural chemicals have unique advantages in inhibiting microglia-mediated neuroinflammation and improving neuronal function. Here, we examined the effects of asperosaponin VI (ASA VI) on LPS-activated primary microglia. Microglia were isolated from mice and pretreated with different doses of ASA VI, following lipopolysaccharide (LPS) administration. Activation and inflammatory response of microglia cells were evaluated by real-time fluorescence quantitative polymerase chain reaction (q-PCR), immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). Signaling pathways were detected by western blotting. We found that the ASA VI inhibited the morphological expansion of microglia cells, decreased the expression and release of proinflammatory cytokines, and promoted the expression of antiinflammatory cytokines in a dose-dependent manner. ASA VI also activated PPAR-γ signaling pathway in LPS-treated microglia. The anti-inflammatory effects of ASA VI in microglia were blocked by treating PPAR-γ antagonist (GW9662). These results showed that ASA VI promote the transition of microglia cells from proinflammatory to anti-inflammatory by regulating PPAR-γ pathway.

小胶质细胞是神经炎症的主要介质。小胶质细胞的活化通常加重了各种神经系统疾病的病理过程。天然化学物质在抑制小胶质细胞介导的神经炎症和改善神经元功能方面具有独特的优势。在这里，我们检查了Asperosaponin VI（ASA VI）对LPS激活的初级小胶质细胞的作用。从小鼠中分离出小胶质细胞，并在脂多糖（LPS）给药后用不同剂量的ASA VI进行预处理。小胶质细胞的激活和炎症反应通过实时荧光定量聚合酶链反应（q-PCR），免疫组化和酶联免疫吸附测定（ELISA）进行评估。通过蛋白质印迹检测信号传导途径。我们发现，ASA VI抑制小胶质细胞的形态扩展，降低促炎细胞因子的表达和释放，并以剂量​​依赖的方式促进抗炎细胞因子的表达。ASA VI还激活了LPS处理的小胶质细胞中的PPAR-γ信号通路。通过治疗PPAR-γ拮抗剂（GW9662），可以阻断ASA VI在小胶质细胞中的抗炎作用。这些结果表明，ASA VI通过调节PPAR-γ途径促进小胶质细胞从促炎性转变为抗炎性。通过治疗PPAR-γ拮抗剂（GW9662），可以阻断ASA VI在小胶质细胞中的抗炎作用。这些结果表明，ASA VI通过调节PPAR-γ途径促进小胶质细胞从促炎性转变为抗炎性。通过治疗PPAR-γ拮抗剂（GW9662），可以阻断ASA VI在小胶质细胞中的抗炎作用。这些结果表明，ASA VI通过调节PPAR-γ途径促进小胶质细胞从促炎性转变为抗炎性。