Kiser Cagla, Gonul Ceren Perihan, Genc Sermin
Izmir Biomedicine and Genome Center, Dokuz Eylul University Health Campus, Mithatpasa St. 58/5 Balcova, 35340 Izmir, Turkey.
Izmir International Biomedicine and Genome Institute, Dokuz Eylul University, Izmir, Turkey.
Cytotechnology. 2024 Apr;76(2):197-208. doi: 10.1007/s10616-023-00609-8. Epub 2023 Nov 28.
Microglia are the tissue-resident immune cells of the central nervous system. As a part of the innate immune response, NLR Family Pyrin Domain Containing Protein 3 (NLRP3) inflammasome activation leads to cleavage of caspase-1 and triggers secretion of proinflammatory cytokines and may also result in pyroptotic cell death. Inflammasome activation plays a crucial role in inflammatory conditions; aberrant activation of inflammasome contributes to the pathogenesis of neurodegenerative diseases. Diethyl Maleate (DEM) is a promising antiinflammatory chemical to alleviate inflammasome activation. In this study, NLRP3 inflammasome was activated in N9 murine microglia via 1 µg/ml LPS (Lipopolysaccharide) for 4 h and 5 mM ATP (Adenosine 5'-triphosphate) for 1 h, respectively. We demonstrated that 1 h pretreatment of DEM attenuated NLRP3 inflammasome activation in microglial cells. Besides, mitochondrial ROS decreased upon DEM pretreatment in inflammasome-induced cells. Likewise, it ameliorated pyroptotic cell death in microglia. DEM is a potent activator of Nrf2 transcription factor, the key regulator of the antioxidant response pathway. Nrf2 has been a significant target to decrease aberrant inflammasome activation through the antioxidant compounds, including DEM. Here, we have shown that DEM increased Nrf2 translocation to the nucleus, resulting in Nrf2 target gene expression in microglia. In conclusion, DEM is a promising protective agent against NLRP3 inflammasome activation.
小胶质细胞是中枢神经系统中的组织驻留免疫细胞。作为固有免疫反应的一部分,含NLR家族pyrin结构域蛋白3(NLRP3)炎性小体的激活会导致半胱天冬酶-1的裂解,并触发促炎细胞因子的分泌,还可能导致细胞焦亡。炎性小体的激活在炎症状态中起关键作用;炎性小体的异常激活会导致神经退行性疾病的发病机制。马来酸二乙酯(DEM)是一种有前景的抗炎化学物质,可减轻炎性小体的激活。在本研究中,分别通过1μg/ml脂多糖(LPS)处理4小时和5mM三磷酸腺苷(ATP)处理1小时,在N9小鼠小胶质细胞中激活NLRP3炎性小体。我们证明,DEM预处理1小时可减弱小胶质细胞中NLRP3炎性小体的激活。此外,在炎性小体诱导的细胞中,DEM预处理后线粒体活性氧减少。同样,它改善了小胶质细胞中的细胞焦亡。DEM是Nrf2转录因子的有效激活剂,Nrf2是抗氧化反应途径的关键调节因子。Nrf2一直是通过包括DEM在内的抗氧化化合物减少异常炎性小体激活的重要靶点。在这里,我们表明DEM增加了Nrf2向细胞核的转位,导致小胶质细胞中Nrf2靶基因的表达。总之,DEM是一种有前景的针对NLRP3炎性小体激活的保护剂。