Propofol Inactivates NF-?B Pathway to Inhibit Lipopolysaccharide-Induced Myocarditis via miR-142-5p/SOCS1 Axis

Purpose: Propofol is a sedative and hypnotic drug widely used in inducing and maintaining anesthesia. Previous studies have shown that propofol has an inhibitory effect on several types of inflammation, but its use in the treatment of myocarditis has not been reported. This study explored the therapeutic effect of propofol on lipopolysaccharide (LPS)-induced myocarditis. Methods: H9c2 cells (embryonic rat cardiomyocytes) were treated with LPS to induce inflammation, and then treated with propofol or transfected with miR-142-5p mimic or inhibitor. The cells were divided into control, LPS, LPS+propofol, LPS+propofol+ negative control (NC) mimic and LPS+propofol+miR mimic groups. Quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) was utilized to measure the relative level of miR-142-5p and suppressor of cytokine signaling 1 (SOCS1). Cell viability and apoptosis were further detected to investigate the efficacy of propofol. SOCS1 and the nuclear factor-kappaB (NF-?B) pathway-related protein levels were quantified using western blot. Results: LPS significantly increased the levels of inflammatory factors, and apoptosis rate in H9c2 cells (p < 0.05). Propofol ameliorated the LPS-induced H9c2 cell damage by inhibiting miR-142-5p. SOCS1 was proved to be directly regulated by miR142-5p. Furthermore, propofol inactivated the NF-?B pathway and increased SOCS1 level by decreasing miR-142-5p expression (p < 0.05). Conclusions: Propofol regulated miR-142-5p/SOCS1 axis to exert anti-inflammatory and cell-activating properties in LPSinduced myocarditis by inactivating the NF-?B pathway.