MicroRNA-124 Prevents H<sub>2</sub>O<sub>2</sub>-Induced Apoptosis and Oxidative Stress in Human Lens Epithelial Cells via Inhibition of the NF-κB Signaling Pathway

<b><i>Aim:</i></b> To investigate the regulation of microRNA-124 ­(miRNA-124) on NF-κB pathway from H₂O₂-induced apoptosis and oxidative stress in human lens epithelial cells (hLEC). <b><i>Methods:</i></b> The MTT (3-[4, 5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide) assay was used to detect hLEC ­viability. HLECs were divided into Blank, H₂O₂, mimics (miRNA-124 mimics) + H₂O₂, NC+ H₂O₂, pyrrolidine dithiocarbamate (PDTC; NF-κB signaling pathway inhibitor) + H₂O₂, and inhibitors (miRNA-124 inhibitors) + PDTC + H₂O₂ groups. Quantitative real-time polymerase chain reaction and Western blot were employed to detect mRNA and protein expressions, Dichloro-dihydro-fluorescein diacetate to measure reactive oxygen species (ROS) production, and AnnexinV-FITC/PI staining to determine cell apoptosis. The mitochondrial membrane potential (MMP) was detected by fluorescence probe JC-1. <b><i>Results:</i></b> The H₂O₂-induced hLEC showed reductions in cell viability with decreased miRNA-124 but increased p-p65 in a dose-/time-dependent manner. Furthermore, ROS production, malondialdehyde content, Bax and Caspase-3 expressions, and cell apoptosis were elevated in H₂O_2-induced hLEC, whereas the activities of superoxide dismutase and glutathione peroxidase, Bcl-2 expression, MMP, as well as the mitochondrial energy metabolism genes were reduced. Additionally, miRNA-124 mimics and PDTC both decreased the p-p65 and reversed the cytotoxicity in H₂O₂-induced hLEC. <b><i>Conclusion:</i></b> MiRNA-124 prevents H₂O₂-induced oxidative stress and apoptosis in hLEC through suppressing the activation of the NF-κB pathway.