Abstract
Spinal cord injury (SCI) is a refractory disease often accompanied by inflammation. Long non-coding RNA NEAT1 (lncRNA NEAT1) was reported to be involved in the expression of the inflammasomes, while the regulatory effect of NEAT1 on SCI was poorly investigated. Herein, we carried out further studies on the pathogenesis of SCI. PC-12 cells were incubated with lipopolysaccharide (LPS) to induce inflammation. Western blotting assay was used to measure the protein expression levels. RNA expression levels were analyzed using RT-qPCR. Cell counting kit 8 and flow cytometry assays were used to separately determine the cell viability and apoptosis rate. The targeted relationships were verified by luciferase reporter and RNA pull-down assays. It was found that LPS induced inflammation in the PC-12 cells, leading to significantly higher cell apoptosis rate and lower viability, and the expression level of NEAT1 was elevated by LPS. However, knockdown of NEAT1 partially reversed the effects of LPS. Subsequently, the potential interaction between NEAT1 and miR-211-5p was validated and miR-211-5p inhibitor was further confirmed to antagonize the effects of NEAT knockdown. The downstream target gene of miR-211-5p was predicted and verified to be MAPK1. In addition, overexpression of MAPK1 was proved to antagonize the effects of NEAT1 knockdown. Taken together, the knockdown of NEAT1 remarkably alleviated the inflammation of SCI via miR-211-5p/MAPK1 axis.