کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5745769 1618781 2018 11 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
PM2.5 exposure stimulates COX-2-mediated excitatory synaptic transmission via ROS-NF-κB pathway
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست شیمی زیست محیطی
پیش نمایش صفحه اول مقاله
PM2.5 exposure stimulates COX-2-mediated excitatory synaptic transmission via ROS-NF-κB pathway
چکیده انگلیسی


- PM2.5 elevated COX-2 expression in primary cultured hippocampal neurons.
- PM2.5 increased COX-2 expression and fEPSP amplitude in hippocampal brain slices.
- PM2.5 exposure potentiated ROS generation and NF-κB phosphorylation.
- PM2.5 disrupted COX-2 mediated synaptic transmission via the ROS-NF-κB pathway.

Long-term exposure to fine particulate matter (PM2.5) has been reported to be closely associated with the neuroinflammation and synaptic dysfunction, but the mechanisms underlying the process remain unclear. Cyclooxygenase-2 (COX-2) is a key player in neuroinflammation, and has been also implicated in the glutamatergic excitotoxicity and synaptic plasticity. Thus, we hypothesized that COX-2 was involved in PM2.5-promoted neuroinflammation and synaptic dysfunction. Our results revealed that PM2.5 elevated COX-2 expression in primary cultured hippocampal neurons and increased the amplitude of field excitatory postsynaptic potentials (fEPSPs) in hippocampal brain slices. And the administration of NS398 (a COX-2 inhibitor) prevented the increased fEPSPs. PM2.5 also induced intracellular reactive oxygen species (ROS) generation accompanied with glutathione (GSH) depletion and the loss of mitochondrial membrane potential (MMP), and the ROS inhibitor, N-acetyl-L-cystein (NAC) suppressed the COX-2 overexpression and the increased fEPSPs. Furthermore, the nuclear factor kappa B (NF-κB) was involved in ROS-induced COX-2 and fEPSP in response to PM2.5 exposure. These findings indicated that PM2.5 activated COX-2 expression and enhanced the synaptic transmission through ROS-NF-κB pathway, and provided possible biomarkers and specific interventions for PM2.5-induced neurological damage.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemosphere - Volume 190, January 2018, Pages 124-134
نویسندگان
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