Knockdown of circular RNA circZNF652 remits LPS-induced inflammatory damage by regulating miR-181a

Background: Infantile pneumonia (IP) is a usual disease in infants and young children. The function and underlying mechanism of circZNF652 on lipopolysaccharide (LPS)-triggered inflammatory damage in WI-38 cells were detected in this article.

Methods: WI-38 cells were induced by dosages of LPS to construct inflammatory injury model. WI-38 cell viability and Apoptosis were detected by CCK-8 assay and flow cytometry, respectively. CircZNF652 and miR-181a levels were changed and detected by Cell Transfection and qRT-PCR. The levels of Apoptosis and JNK/p38 and NF-κB pathways-related proteins, as well as the level of COX-2 were detected by western blot. Finally, the concentrations of inflammatory factors were detected by ELISA.

Results: LPS induced inflammatory injury showing as notably decreased the viability, while increased the numbers of apoptotic cells, as well as the levels of Apoptosis and inflammatory factors in a dose dependent way. Besides, LPS inducement remarkably enhanced the expression of circZNF652. However, knockdown of circZNF652 remitted LPS-triggered inflammatory damage and restrained NF-κB and JNK/p38 pathways. Moreover, circZNF652 knockdown promoted miR-181a expression. Whereas, miR-181a inhibition markedly relieved circZNF652 knockdown-induced impacts.

Conclusion: Knockdown of circZNF652 remitted LPS-triggered WI-38 cells inflammatory damage through deactivation of NF-κB and JNK/p38pathways by up-regulating miR-181a.