Abstract：
This study designed to investigate the potential role of lncRNA NEAT1/miR-146b in infantile pneumonia. In this study, 58 children with pneumonia and 58 healthy children collected for routine examination from December 2016 to January 2019. The lncRNA NEAT1 and miR-146b expression levels were detected by qPCR in both groups. The pneumonia model was established by inducing human embryonic lung fibroblasts HFL1 with LPS, and then transfected with lncRNA NEAT1 inhibition and miR-146b over-expression vector to observe the effect on cell viability and apoptosis after induction. Starbase predicted the binding site between lncRNA NEAT1 and miR-146b, and the targeted relationship between them was detected by dual luciferase reporter gene. The relative expression of lncRNA NEAT1 in serum of infantile pneumonia was up-regulated. Knocking down lncRNA NEAT1 promotes cell growth and reduces apoptosis in LPS-induced HFL1 cells. Results showed that the fluorescence activity of lncRNA NEAT1 obviously reduced when combined with miR-146b. In conclusion, the relative expression of miR-146b in serum of infantile pneumonia decreased, and over-expressing it could promote LPS-induced cell viability and reduce apoptosis. Taken together, this study demonstrated that the lncRNA NEAT1 regulates infantile pneumonia by sponging miR-146b.
摘要：
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