Inhibition of lincRNA-Cox2 alleviates apoptosis and inflammatory injury of lipopolysaccharide- stimulated human bronchial epithelial cells via the Nrf2/HO-1 axis

This study mainly explored the role and mechanism of lincRNACox2 in inflammatory injury of human bronchial epithelial cells. BEAS-2B cells were stimulated with lipopolysaccharide to establish an in vitro inflammatory injury model. Real-time polymerase chain reaction was used to detect lincRNA-Cox2 expression in LPS-stimulated BEAS-2B. Cell viability and apoptosis of cells were assessed using CCK-8 and Annexin V-PI double staining. The contents of inflammatory factors were determined by enzyme-linked immunosorbent assay kits. The protein levels of nuclear factor erythrocyte 2-related factor 2 and haem oxygenase 1 protein levels were measured by Western blot. The results showed that lincRNA-Cox2 was upregulated in LPS-stimulated BEAS-2B cells. lincRNA-Cox2 knockdown inhibited apoptosis and the release of tumour necrosis factor alpha, interleukin ]beta (IL-113), IL-4, IL-5, and IL-13 in BEAS-2B cells. lincRNA-Cox2 overexpression had the opposite effect. lincRNA-Cox2 knockdown also inhibited LPS-induced oxidative damage in BEAS-2B cells. Further mechanistic studies showed that inhibition of lincRNACox2 upregulated the levels of Nrf2 and HO-1, and si-Nrf2 reversed the effects of si-lincRNA-Cox2. In conclusion, lincRNACox2 knockdown inhibited BEAS-2B apoptosis and the level of inflammatory factors by activating the Nrf2/HO-1 pathway.