Knockdown of circ_0038467 alleviates lipopolysaccharides-induced 16HBE cell injury by regulating the miR-545-3p/TRAF1 axis in neonatal pneumonia

Background: Neonatal pneumonia is a common illness in the neonatal period with a high fatality rate. Accu-mulating proofs have attested to the crucial role of circular RNAs (circRNAs) in pneumonia. This study was intended to expound on the function of circ_0038467 and the underlying mechanism in lipopolysaccharide (LPS)-stimulated 16HBE cell injury in neonatal pneumonia.Methods: 16HBE cells were exposed to LPS to establish an in vitro neonatal pneumonia cell model. Quantitative real-time polymerase chain reaction (qRT-PCR) was implemented for detecting the levels of circ_0038467, microRNA-545-3p (miR-545-3p), and tumor necrosis factor receptor-associated factor 1 (TRAF1) in neonatal pneumonia serums and LPS-treated 16HBE cells. Cell Counting Kit-8 (CCK-8), 5-ethynyl-2 '-deoxyuridine (EdU) incorporation, and flow cytometry assays were used to examine cell viability, proliferation, and apoptosis, respectively. The protein abundances of proliferation/apoptosis/inflammation-correlated makers and TRAF1 were tested by Western blot. RNase R and Actinomycin D assays were implemented to determine the features of circ_0038467. The mutual effect between miR-545-3p and circ_0038467 or TRAF1 was affirmed by a dual-luciferase reporter and RNA pull-down assay assays. Results: Circ_0038467 was upregulated in neonatal pneumonia serum specimens and LPS-triggered 16HBE cells. LPS administration restrained 16HBE cell proliferation and promoted apoptosis and inflammation, whereas circ_0038467 silence recovered these influences. Meanwhile, miR-545-3p was targeted by circ_0038467, and circ_0038467 could modulate LPS-treated 16HBE cell injury through absorbing miR-545-3p. Furthermore, circ_0038467 controlled TRAF1 level via segregating miR-545-3p. Moreover, TRAF1 overexpression relieved the suppressive impact of circ_0038467 silence in LPS-triggered 16HBE cell detriment.Conclusion: Circ_0038467 knockdown mitigated LPS-exposed 16HBE cell damage through regulating miR-545-3p/PPARA axis.