Endoplasmic Reticulum Stress and NLRP3 Inflammasome Activation Underlie Silver Nanoparticles-Induced Neurologic Deficits in Adult Mice

Abstract

Silver nanoparticles (AgNPs) are extensively mass-produced and widely utilized across diverse fields owing to their potent bactericidal properties. Nevertheless, prior research regarding the distribution of AgNPs In Vivo has revealed that they can penetrate into and accumulate in brain tissue, potentially leading to neurotoxicity. In the current study, we initially delved into the impacts of different dosages of AgNPs (10−250 mg/kg body weight) on behavioral cognitive function. After 28 days of oral ingestion of AgNPs, we observed impaired learning and memory performance in the high-dose-treated group of mice. Moreover, we evaluated the alterations in molecules associated with endoplasmic reticulum (ER) stress and the activation of the NOD-like receptor protein 3 (NLRP3) inflammasome, conducting a preliminary exploration of the neurotoxic mechanisms of AgNPs. The results demonstrated that subacute oral exposure to AgNPs might disrupt cognitive function via the ER stress and NLRP3 inflammasome activation pathways. Our data highlight the neurotoxic effects of AgNPs and the significant role played by NLRP3 inflammasome activation in neurological deficits.