Abstract
Neonatal pneumonia is a high neonatal mortality disease. We studied the function and mechanism of long noncoding RNA myocardial infarction-associated transcript 2 (lncRNA MIAT2) on lipopolysaccharide (LPS)-induced inflammation in WI-38 cells. Cell Counting Kit-8 and apoptosis assay were respectively used to detect the functions of LPS, MIAT2, and microRNA-15 (miR-15) on viability and apoptosis. MIAT2 and miR-15 expressions were changed by cell transfection. Moreover, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), western blot, and enzyme-linked immunosorbent assay were used to detect the expressions of interleukin (IL)-6 and monocyte chemoattractant protein-1 (MCP-1). The levels of Bax, cleaved-caspase-3, and cell pathways-related proteins were tested by western blot. Besides, the levels of miR-15 and MIAT2 were tested by RT-qPCR. We found that LPS declined cell viability and heightened apoptosis and levels of Bax, cleaved-caspase-3, IL-6, and MCP-1. MIAT2 was negatively regulated by LPS and it alleviated LPS-induced damage. Furthermore, MIAT2 reversely regulated miR-15 and miR-15 mimic could reverse the effects of MIAT2. Finally, MIAT2 restrained the p38MAPK and NF-κB pathways by downregulating miR-15. In conclusion, MIAT2 alleviated LPS-induced inflammation damage in WI-38 cells by sponging miR-15 via p38MAPK and NF-κB pathways.