Ischemia-reperfusion (IR) injury is a major cause of clinical emergencies during and after surgical procedures.Propofol protects the heart from cardiovascular IR injury by inhibiting autophagy. MicroRNAs (miRNAs)participate in anesthetic-regulated cardiovascular injury. MiR-20b-5p targets unc-51-like autophagy activatingkinase 1 (ULK1). Its role in propofol-modulated cardiovascular IR injury remains unclear, however. In thisstudy, we used an in vitro model of hypoxia-reoxygenation (HR)-induced injury to human umbilical veinendothelial cells (HUVECs) to determine the protective effect of miR-20b-5p in cells preconditioned withpropofol. We found that miR-20b-5p was significantly higher and ULK1 was lower in propofol-preconditionedHUVECs with HR injury than in HUVECs with HR injury only. Additionally, miR-20b-5p overexpressionincreased cell viability and repressed autophagy and apoptosis more in propofol-preconditioned HUVECs withHR injury than in HUVECs with HR injury only. A luciferase reporter assay confirmed the target reactionbetween miR-20b-5p and ULK1. Overexpression of ULK1 restrained the protective effect of miR-20b-5p inpropofol-preconditioned HUVECs with HR injury. In conclusion, our results indicate that propofol inhibitsautophagic cell death via the miR-20b-5p-ULKI axis and that ULK1 may be a therapeutic target for cardiovascularIR injury.
Volume 47, 2022
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