MicroRNA-218 Inhibits Lipopolysaccharide-Induced Bronchial Epithelial Cell Injury by Targeting E2F2

Abstract

Acute bronchopneumonia is a common hospitalization disease in children and serious acute bronchopneumonia will lead to death of children. MicroRNAs (miRNAs) have been thought to be related to inflammation in many diseases. The present study aimed to investigate the relation between miR218 and E2F2 and the effect of miR-218 overexpression and E2F2 inhibition on the improvement of inflammation in LPS-induced bronchial epithelial cell. BEAS-2B cells were induced by LPS for 0, 6, 12, 24 and 48 h which the cell viability was analyzed by CCK-8 assay. The expression of miR-218 in LPS-induced bronchial epithelial cell and cell transfection was detected by RT-qPCR analysis. The levels of TNF-α, IL-1α, and IL-6 in BEAS2B cells were detected using commercially-available ELISA kits. The levels of ROS, MDA, SOD and LDH were detected by ROS assay kit and oxidative stress assay kit. The cell apoptosis was analyzed by flow cytometry analysis and DAPI and hochest staining. As a result, miR-218 was decreased in LPS-induced bronchial epithelial cell. With the time of LPS treatment extends, the cell viability was decreased. Overexpression of miR-218 reduced the expression of inflammatory cytokines and oxidative stress injury in LPS-induced BEAS2B cells. Overexpression of miR-218 reduced apoptosis of LPS-induced BEAS2B cells. E2F2 was demonstrated be a target of miR-218 which miR-218 overexpression could inhibit the expression of E2F2. E2F2 inhibition could reverse the inflammatory and oxidative stress injury of LPS-induced BEAS2B cells caused by miR-218 inhibition. E2F2 inhibition could reverse the apoptosis of LPS-induced BEAS2B cells caused by miR-218 inhibition. In addition, E2F2 inhibition could reverse the expression of p-STAT1, cleaved-caspase3 and cleaved-caspase9 in LPS-induced BEAS2B cells caused by miR-218 inhibition. In conclusion, this study indicated that miR-218 overexpression and E2F2 inhibition can alleviate the inflammation in LPS-induced bronchial epithelial cell, thereby decreasing the oxidative stress and cell apoptosis.