Particulate matter(PM(2.5)) exposure season-dependently induces neuronal apoptosis and synaptic injuries

摘要

Epidemiological studies have shown that particulate matter 2.5(PM_(2.5)) not only increases the incidence of cardiopulmonary illnesses but also relates to the development of neurodegenerative diseases. Considering that PM_(2.5)is highly heterogeneous with regional disparity and seasonal variation, we investigated whether PM_(2.5)exposure induced neuronal apoptosis and synaptic injuries in a season-dependent manner. The results indicated that PM_(2.5)altered the expression of apoptosis-related proteins(mainly bax and bcl-2), activated caspase-3 and caused neuronal apoptosis. Additionally, PM_(2.5)decreased the levels of synaptic structural protein postsynaptic density(PSD-95) and synaptic functional protein N-methyl-D-aspartate(NMDA) receptor subunit(NR2B) expression. These effects occurred in a season-dependent manner, and PM_(2.5)collected from the winter showed the strongest changes. Furthermore, the effect was coupled with the inhibition of phosphorylated extracellular signal-regulated kinase 1/2(p-ERK1/2) and phosphorylated c AMP-response element binding protein(p-CREB). Based on the findings, we analyzed the correlations between the chemical composition of PM_(2.5)samples and the biological effects, and confirmed that winter PM_(2.5)played a major role in causing neuronal apoptosis and synaptic injuries among different season samples.