Silver nanoparticles induce damage in BV2 microglia via the mitochondrial dysfunction-PINK1/Parkin signaling pathway.

Research remains limited regarding the potential mechanisms by which silver nanoparticle (AgNPs) induced nerve injury, specifically mitochondrial damage in microglia. This study investigates the mitochondrial damaging effects of AgNPs in BV2 cells. BV2 cells were treated with AgNPs to evaluate their impact. Their mitochondrial morphological alterations were observed via transmission electron microscopy, and mitochondrial functional changes were assessed using various assays, including JC-1 labeling, ATP measurement, mitochondrial reactive oxygen species (mtROS) detection. The result demonstrated that BV2 cells treated with AgNPs showed vacuolization, damaged mitochondrial cristae, and even ruptured the outer membrane. In addition, AgNPs leads BV2 cells mitochondrial membrane to potential collapsed, marked elevation of total cellular ROS and mtROS, and reduced their ATP production. Furthermore, the mitochondrial division inhibitor-1 effectively reduced the rise in mitochondrial fission caused by AgNPs. Interestingly, it also reduced the mtROS, the activation of PINK1/Parkin pathway, and apoptosis caused by AgNPs. These results clearly demonstrated that AgNPs triggered neurotoxicity by targeting mitochondria which disrupts mitochondrial homeostasis. Our study shows that AgNPs induce neurotoxicity in BV2 cells through the activation ofmitochondrial dysfunction-PINK1/Parkin signaling pathway. These findings offer novel insights into the mechanisms underlying AgNPs-induced neurotoxicity, which could present potential strategies to lessen their harmful consequences.