The liver, an organ with robust regenerative capacity, is involved in many physiological functions, such as detoxification and modulation of optimal brain function. Exosomes are secreted by almost all cell types and mediate intercellular communication, as well as, they are involved in neuroinflammatory process. In this study, we found that fetal liver cell-derived exosomes (FLC-EXOs) administration to lipopolysaccharide (LPS)-induced microglia, which are brain resident immune cells responsible for neuroinflammation, decreased the expression of pro-inflammatory cytokines, such as interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), in the LPS-activated microglia. We also examined the different signaling pathways that may be involved in this process to determine the anti-inflammatory mechanism of FLC-EXOs. The results showed that activation of the p38 pathway was attenuated after FLC-EXOs administration, which may be related to the anti-inflammatory effects of FLC-EXOs.

肝脏是一种具有强大再生能力的器官，参与许多生理功能，例如解毒和调节最佳大脑功能。外泌体几乎由所有细胞类型分泌并介导细胞间通讯，并且它们参与神经炎症过程。在这项研究中，我们发现胎肝细胞衍生的外泌体（FLC-EXOs）对脂多糖（LPS）诱导的小胶质细胞（负责神经炎症的大脑驻留免疫细胞）给药，降低了促炎细胞因子的表达，如白细胞介素-1β (IL-1β) 和肿瘤坏死因子-α (TNF-α)，在 LPS 激活的小胶质细胞中。我们还检查了可能参与该过程的不同信号通路，以确定 FLC-EXO 的抗炎机制。