槐果碱通过AMPK/Nrf-2/HO-1-NF-κB信号传导途径抑制LPS诱导的小胶质细胞细胞炎症反应

Sophocarpine inhibits LPS-induced microglial cell inflammatory response via AMPK/Nrf-2/HO-1-NF-κB signaling

神经炎症是脑和脊髓中小胶质细胞和星形胶质细胞过度活化而激活的免疫应答,其在神经退行性疾病的发病过程中发挥着至关重要的作用。激活后,小胶质细胞会产生多种炎症介质,引发过度的炎症反应,并最终破坏周围的神经元。因此,可以通过抑制小胶质细胞的过度活化,从而抑制神经炎症的药物具有治疗神经退行性疾病的潜力。槐果碱对中枢神经系统具有抑制作用,具有抑制急性渗出性炎症和弱镇痛作用,但尚未见报道槐果碱是否可以抑制神经炎症。本试验以小胶质细胞系BV-2为对象,研究槐果碱对LPS诱导的小胶质细胞炎症反应的影响及其机制。结果表明,槐果碱通过AMPK/Nrf-2/HO-1-NF-κB信号传导途径抑制LPS诱导的小胶质细胞中的炎症反应。

Neuroinflammation is an immune response featured with excessive activation of microglia and astrocytes in the brain and spinal cord,and it plays a vital role in the pathogenesis of neurodegenerative diseases.After activation,microglia produces several kinds of inflammatory mediators,triggers an excessive inflammatory response,and ultimately destroys the surrounding neurons.Therefore,agents that can inhibit the excessive activation of microglia and inhibit neuroinflammation have a potential to treat neurodegenerative diseases.Sophocarpine has an anti-inflammatory effect on the central nervous system,and can inhibit acute exudative inflammation and weak analgesia.However,whether sophocarpine exerts the same function in neuroinflammation is not known.In the present study,we aimed to study the effects and mechanisms of sophocarpine as an anti-inflammatory drug candidate in LPS-stimulated BV-2 cells.Hence,these findings demonstrate that sophocarpine suppresses neuroinflammation caused by overactivated microglia via regulating the AMPK/Nrf-2/HO-1-NF-κB signaling axis.