Long Noncoding RNA DLIC Reduces Inflammation, Oxidative Stress and Apoptosis in Lung Epithelial Cells Induced by Lipopolysaccharide (LPS)

Abstract

The effective improvement of acute lung injury (ALI) plays an important role in reducing the mortality of sepsis. LncRNA was expressed abnormally in inflammatory diseases and restoration of lncRNA could improve the inflammatory injury. However, the protective effects of DLIC on ALI, as well as the regulatory mechanism of DLIC in ALI are still unknown. LPS-induced lung epithelial cells were constructed in vitro to simulate the ALI model. The expression of DLIC in lung epithelial cells and DLIC transfection effects were analyzed by RT-qPCR analysis. The cell viability and cell apoptosis were respectively detected by CCK-8 assay and flow cytometry analysis. The expression of inflammatory factors and oxidative stress factors was determined by the commercial assay kits. The expression of apoptosis-related proteins and TLR4/NF-κB pathway-related proteins was analyzed by western blot analysis. As a result, DLIC expression was decreased in LPS-induced BEAS-2B cells. DLIC overexpression improved the cell viability and inhibited the apoptosis of LPS-induced BEAS-2B cells with the changes of protein expression. DLIC overexpression alleviated the inflammation and oxidative stress by depressing the levels of inflammatory factors and oxidative stress factors. Furthermore, DLIC overexpression inhibited TLR4/NF-κ B pathway. In conclusion, DLIC reduces inflammation, oxidative stress and apoptosis in LPS-induced BEAS-2B cells by suppressing TLR4/NF-κB pathway.