Circ-Phkb promote LPS-induced acute lung injury via the TLR4/MyD88/NF-?B /CCL2 axis
Our results showed that both circRNA and mRNA profiles are different from those of the sham group. A significant upregulation of circ-Phkb was observed in NR8383 cells and rats exposed to LPS. When circ-Phkb expression was reduced in NR8383 cells, apoptosis and inflammation were greatly reduced, and cell proliferation was increased, while overexpression of circ-Phkb have the opposite effect. In terms of mechanism, circ-Phkb suppression inhibits CCL2 expression via TLR4/MyD88/NF-?B pathway. Overall design: In this study, we obtained differential circRNA and mRNA expression profiles and possible ceRNA networks through circRNA sequencing, mRNA sequencing and bioinformatics analysis of lung tissues from an LPS-induced ALI rat model. Furthermore, qRT-PCR assays were performed to screen for circ-Phkb in ALI rat lung tissues, alveolar macrophages and LPS-induced NR8383 cells. Induction with or without LPS was then conducted with circ-Phkb siRNA and overexpression lentivirus in NR8383. Proliferation was detected by CCK8 and Edu staining, and apoptosis was detected by TUNEL assay and cytometry. Inflammatory factors were detected using ELISA. Finally, WB was used to detect the apoptosis-related proteins and the activation of the TLR4/MyD88/NF-?B pathway.