Background: Propofol is an anesthetic agent and can impede the progression of human diseases. Circular RNA (circRNA) circ_0003645 has been identified to promote the development of atherosclerosis (AS). This study aimed at the functional mechanism of propofol and circ_0003645 in AS.
Methods: AS cell model was established by treatment of oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells (HUVECs). Cell viability or apoptosis detection was performed by Cell Counting Kit-8 (CCK-8) assay and flow cytometry. Circ_0003645, microRNA-149-3p (miR-149-3p) and tumor necrosis factor receptor-associated factor 7 (TRAF7) levels were determined by the quantitative real-time polymerase chain reaction (qRT-PCR). Inflammatory cytokines were examined using enzyme-linked immunosorbent assay (ELISA). Protein analysis was conducted by western blot. The interaction of miR-149-3p and circ_0003645 or TRAF7 was analyzed using dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay.
Results: Treatment of ox-LDL inhibited cell viability and enhanced apoptosis in HUVECs to establish the AS cell model. Propofol protected against cell viability inhibition and apoptosis promotion in AS cell model. Circ_0003645 expression was downregulated by propofol in AS cell model. Propofol alleviated cell apoptosis and inflammation by decreasing the circ_0003645 level. Circ_0003645 targeted miR-149-3p, and circ_0003645/miR-149-3p axis was involved in the functional regulation of propofol. TRAF7 was the target of miR-149-3p. Inhibition of miR-149-3p affected the function of propofol by upregulating the TRAF7 expression. Circ_0003645 sponged miR-149-3p to induce the upregulation of TRAF7 following propofol treatment.
Conclusion: It has been suggested that propofol acted as an inhibitor against the ox-LDL-induced cell injury by the circ_0003645/miR-149-3p/TRAF7 axis.
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| http://dx.doi.org/10.3233/CH-221437 | DOI Listing |
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