LAUSR

This study aimed to explore the mechanism of miR-320 in regulating biological characteristics of ischemic cerebral neuron by mediating Nox2/ROS pathway. Primary neurons were cultured and grouped: normal group (normal primary neurons), negative control (NC) group (ischemic primary neurons, transfected with negative control plasmid), model group (ischemic primary neurons), miR-320 mimic group (ischemic primary neurons, transfected with miR-320-overexpressed plasmid), Nox2 vector group (ischemic primary neurons, transfected with Nox2-overexpressed plasmid), and miR-320 mimic + Nox2 vector group (ischemic primary neurons, co-transfected with miR-320- and Nox2-overexpressed plasmid). Dual-luciferase reporter assay showed that there was the target relationship between miR-320 and Nox2. miR-320 expression was significantly decreased, and Nox2 expression was significantly increased in the rest groups compared with normal group (both P  < 0.05). There was a co-localization of miR-320 and Nox2 in the cytoplasm. Cell proliferation, contents of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX), and mRNA and protein expressions of Ki67, Bcl-2, and c-myc were significantly declined, and apoptosis rate, contents of malondialdehyde (MDA) and reactive oxygen species (ROS), and caspase-3 mRNA and protein expressions were significantly increased in the rest groups compared with normal group (all P  < 0.05). miR-320 promoted cell proliferation; increased contents of SOD, CAT, and GSH-PX; and declined apoptosis and contents of MDA and ROS. Moreover, miR-320 could affect the regulation of Nox2/ROS pathway on ischemic cerebral neuron by negatively regulating Nox2 expression. Overexpressed miR-320 affects the proliferation, apoptosis, and oxidative stress injury of ischemic cerebral neuron by inhibiting Nox2/ROS pathway.