Propofol inhibits injury of human umbilical vein endothelial cells by regulating the miR-17-activated STAT3 signalling pathway

Fujiang Wei, Jie Zhang^* 

Department of Anesthesia, Yantai Mountain Hospital, Yantai, PR China

Objective: To explore the mechanism by which propofol inhibits injury to human umbilical vein endothelial cells.

Methods: Human umbilical vein endothelial cells (HUVECs) were cultured to establish an oxidative stress cell injury model, and then treated with propofol. HUVECs were divided into a control group, injury group, control + propofol group and injury + propofol group. The expression of miR-17 was detected by real-time fluorescent quantitative PCR. A miR-17 interference plasmid, miR-17 control plasmid and miR-17 overexpression plasmid were transfected into the cells for culture. A miR-17 negative control group, miR-17 low-expression group and miR-17 overexpression group were obtained. The cell activity was determined by the CCK-8 method, apoptosis was detected by flow cytometry, and the expression levels of Bcl-2, Bax and STAT3 were detected by a Western blot. A luciferase reporter assay was used to detect the binding ability of miR-17 to 3'UTR of STAT3.

Results: Compared with the control group, the expression level of miR-17 in the control + propofol group was significantly lower (P < 0.05). Compared with the injury group, the expression level of miR-17 in the injury + propofol group was significantly lower (P < 0.05). Compared with the injury group, the cell activity was significantly increased, the apoptosis rate and Bax expression level were significantly decreased and the Bcl-2 expression level was significantly increased in the injury + propofol group (P < 0.01). Compared with the miR-17 control group, the cell activity, apoptosis rate and Bax and Bcl-2 expression levels in the miR-17 low-expression group were significantly increased (P < 0.01 or P < 0.05). Compared with the miR-17 control group, the expression level of STAT3 in the miR-17 overexpression group was significantly lower (P < 0.05). Compared with the miR-17 negative control group, the luciferase activity of wild-type STAT3 3'UTR in the miR-17 overexpression group was significantly decreased (P < 0.01). There was no significant difference in luciferase activity between the two groups (P > 0.05).

Conclusion: Propofol may inhibit the expression of miR-17 and activate the STAT3 signalling pathway, to promote the proliferation of injured human umbilical vein endothelial cells, inhibit their apoptosis and heal their injuries.