LncRNA MINCR inhibits LPS-induced damage and inflammation of alveolar epithelial cell line A549 by targeting at miR-223

Objective To investigate the potential effects of long non-coding RNA (lncRNA) MINCR on lipopolysaccharide (LPS)-induced human alveolar epithelial cell line A549 damage and inflammation through targeted regulation of miR-223. Methods A549 cells were randomly divided into control group, LPS group, LPS+transfection group(Si NC group, Si MINCR group, miR-223 NC group, miR-223 mimic group, Si NC+miR-223 NC group, Si NC+miR-223 antagomir group, Si MINCR+miR-223 NC group, and Si MINCR+miR-223 antagomir group). RT-qPCR was performed to determine the expression levels of MINCR and miR-223; Flow cytometry was performed to determine the rate of apoptosis; ELISA was performed to determine the levels of serum tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6); Bioinformatics prediction and dual luciferase reporter gene assay were performed to verify the targeting relationship of MINCR and miR-223; Western blot was performed to test the expression levels of activated caspase-3 (cleaved caspase-3) and B-cell lymphoma-2(Bcl-2) proteins in the cells. Results There was a targeting relationship between MINCR and miR-223. Compared with the control group, the apoptosis rate, the level of TNF-α and IL-6, and the expression of MINCR, cleaved caspase-3 proteins in the LPS group were significantly increased (PPPPPPPConclusions Silencing the expression of lncRNA MINCR may target the activation of miR-223 expression, inhibit cell apoptosis and inflammation, and reduce LPS-induced damage of alveolar epithelial cells.