%0 Journal Article
%T Knockdown of circular RNA circZNF652 remits LPS-induced inflammatory damage by regulating miR-181a.
%A Liu X
%A Zhao P
%A Ge W
%J Biofactors
%V 46
%N 6
%D Nov 2020
%M 31889339
%F 6.438
%R 10.1002/biof.1606
%X 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.
CONCLUSIONS: Knockdown of circZNF652 remitted LPS-triggered WI-38 cells inflammatory damage through deactivation of NF-κB and JNK/p38pathways by up-regulating miR-181a.