Astrocytes activation related NF-κB signaling and oxidative stress were treated as key target associated with PM2.5 threating nerve injury. Unfortunately, the underlying molecular mechanisms of interaction between NF-κB signaling, glial cells activation in neuroinflammation are still not absolutely explained. Fisetin, a natural flavonoid was found to be promote health, partly due to its ability in antioxidant and anti-inflammation. In this regard, we constructed fisetin nanoparticles (FN) to investigate the anti-inflammatory effect in PM2.5-induced mice. Accordingly, qPCR and western blot analysis indicated that astrocytes activation related NF-κB signaling and oxidative stress contributed to PM2.5-induced neuroinflammation, which were significantly suppressed by increasing concentration of FN treatment. Also, FN may directly enhance anti-oxidative stress and anti-inflammatory way to perform inhibitory effects on NF-κB related glial cells activation. Overall, here we identified a new mechanism of action of FN as potential anti-inflammatory product against PM2.5-induced neuroinflammation via regulation of astrocytes activation related NF-κB.

星形胶质细胞激活相关的NF-κB信号和氧化应激被视为与PM2.5威胁神经损伤相关的主要靶标。不幸的是，NF-κB信号传导，神经炎中神经胶质细胞活化之间相互作用的潜在分子机制仍未得到绝对解释。非瑟酮（一种天然的类黄酮）被发现可以促进健康，部分原因是它具有抗氧化和抗发炎的能力。在这方面，我们构建了非瑟酮纳米颗粒（FN），以研究在PM2.5诱导的小鼠中的抗炎作用。因此，qPCR和蛋白质印迹分析表明，星形胶质细胞活化相关的NF-κB信号传导和氧化应激促成PM2.5诱导的神经炎症，这被FN处理浓度的增加明显抑制。还，FN可能直接增强抗氧化应激和抗炎作用，从而对NF-κB相关的神经胶质细胞活化产生抑制作用。总体而言，在这里，我们通过调节星形胶质细胞激活相关的NF-κB，确定了FN作为对抗PM2.5诱导的神经炎症的潜在抗炎产品的新作用机制。