Propofol (PRO), a clinical potent intravenous anesthetic, plays a significant role in relieving inflammatory diseases by repressing the release of inflammatory cytokines. The present study was aimed to reveal a novel mechanism by which PRO alleviates acute lung injury (ALI). Lipopolysaccharide (LPS) was utilized to induce human pulmonary microvascular endothelial cells (HPMECs) so as to simulate the microenvironment of ALI, and the expression of apolipoprotein M (APOM) was examined with western blotting. Then, APOM was silenced and profopol was used to treat the LPS-injured HPMECs. The cell viability, migration, and apoptosis were respectively observed after the processes of cell counting kit-8, wound healing, transwell, and TUNEL assay. Meanwhile, the inflammatory response was detected by determining the contents of inflammatory cytokines. Subsequently, the relationship between phosphoinositide-3 kinase (PI3K)/protein kinase B (AKT) signaling pathway and PRO was analyzed by western blotting. PI3K/AKT inhibitor LY294002 was employed to evaluate whether the effects of PRO on LPS-challenged HPMECs injury were mediated by this pathway. Results revealed that APOM was notably downregulated in HPMECs after LPS exposure. PRO treatment promoted cell proliferation and migration while alleviated inflammation and apoptosis of LPS-treated HPMECs, which was reversed by APOM-downregulation. PRO brought about the upregulation of proteins in PI3K/AKT signaling pathway, and LY294002 intervention further accentuated the impacts of APOM-knockdown on LPS-challenged HPMECs injury. To conclude, PRO promotes migration and alleviates inflammation and apoptosis of LPS-treated HPMECs by PI3K/AKT signaling pathway via upregulating APOM, which laid an experimental foundation for the future study and clinical application of PRO.
Keywords: APOM; acute lung injury; apoptosis; inflammation; propofol.
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