Effect of knockdown of long noncoding RNA metastasis associated lung adenocarcinoma transcript 1 on microglial activation

Objective To investigate the effect of down-regulation of human lung adenocarcinoma metastasis-associated transcript 1 (MALAT1) on microglial activation and its possible mechanism. Methods BV2 microglial cells were cultured in vitro and divided into a normal control group (no treatment), a lipopolysaccharide (LPS) treatment group (cultured with 100 ng/mL LPS), a MALAT1 interference group (transfected with MALAT1 interference sequence + cultured with 100 ng/mL LPS) and a control sequence group (transfected with control sequence + cultured with 100 ng/mL LPS). Real-time fluorescence quantitative PCR was used to detect the expression of MALAT1 mRNA in the cells. Western blotting was used to detect the expression of NF-κB protein and IκB-α protein in the cells. Enzyme linked immunosorbent assay (ELISA) was used to detect the levels of IL-1β, IL-6, IL-10 and TNF-α in each group. Nitric acid reduction method (Griess method) was used to detect nitric oxide (NO) concentration in each group. Results The relative expression levels of MALAT1 mRNA and NF-κB protein were significantly increased, the relative expression level of IκB-α protein was significantly decreased, the levels of IL-1β, IL-6, IL-10 and TNF-α and the release of NO in the cell supernatant were significantly increased in the LPS treatment, MALAT1 interference and control sequence groups than in the normal control group (P<0.05). The relative expression levels of MALAT1 mRNA and NF-κB protein were significantly decreased, the expression level of IκB-α protein was significantly increased, the levels of IL-1β, IL-6, IL-10 and TNF-α and the release of NO in the cell supernatant were significantly decreased in the MALAT1 interference group than in the LPS treatment and control sequence groups (P<0.05). Conclusions Down-regulation of MALAT1 gene expression may inhibit the inflammatory response induced by LPS-induced BV2 cell activation. The mechanism might be related to the inhibition of NF-κB signaling pathway. Key words: Metastasis associated lung adenocarcinoma transcript 1; Microglial cells; Inflammatory reaction; NF-κB signaling pathway; Long noncoding RNA