Study on the effect and mechanism of PM2.5 on the expression of Alzheimer’s disease-like pathological proteins in SH-SY5Y cells

Abstract

Fine particulate matter (PM_2.5) is recognized as one of the most harmful environmental pollutants to human health. Current research indicates that PM_2.5 exhibits neurotoxic effects, though the specific mechanisms remain unclear. In this study, SH-SY5Y cells were exposed to PM_2.5 (100 μg/mL for 24 h) to observe its effects on the expression of Alzheimer's disease (AD)-related proteins and explore the possible mechanisms of central nervous system injury caused by PM_2.5. Based on bioinformatics results, the study employed a PI3K inhibitor (LY294002, 10 μmol/L for 1 h) and a reactive oxygen species (ROS) inhibitor, N-acetyl-L-cysteine (NAC, 5 nmol/L for 1 h), as interventions. The results demonstrated that PM_2.5 exposure significantly intensified oxidative stress in SH-SY5Y cells, upregulated the expression of inflammatory factors, and increased apoptosis. Additionally, exposure to PM_2.5 led to elevated levels of AD-related pathological proteins, including amyloid-β (Aβ), and promoted Tau phosphorylation, further indicating its potential neurotoxic effects. Furthermore, the ROS/PI3K/Akt/GSK-3β pathway was found to play a key role in these processes. This research provides a basis for understanding the impact of PM_2.5 on Alzheimer’s disease patients and offers recommendations for the prevention of haze-related health risks, as well as for risk management by relevant governmental departments.