Propofol Inhibits Mircrorna-17 Expression In Vascular Endothelial Cells During Ischemia-Reperfusion

This study is to investigate the role of miR-17 in propofol induced protective effects in vascular endothelial cells. Hypoxia-reoxygenation (H/R) model was established in human umbilical vein endothelial cells (HUVECs) to mimic the in vivo situation of ischemia-reperfusion, and the cells were treated with propofol or not. Expression of miR-17 was analyzed using Real-time PCR. HUVECs were transfected with miR-17 inhibitor or scramble control and subjected to H/R. Cell viability and apoptosis was detected by CCK8 assay and flow cytometry. Western blot was performed to analyze apoptosis-related proteins. Target of miR-17 was predicted by bioinformatics analysis and verified by Dual-luciferase reporter gene assay. Expression of miR-17 was decreased after propofol treatment. Blocking endogenous miR-17 significantly increased cell viability and decreased apoptosis rate, which was consistent with the effect of propofol treatment. Blocking miR-17 expression and propofol treatment after H/R inhibited the expression of Bax but upregulated Bcl-2 expression. In addition, 3' untranslated region (3' UTR) of signal transducer and activator of transcription 3 (STAT3) has a putative binding site for miR-17. MiR-17 was able to directly bind to the STAT3 3' UTR and negatively regulate the expression of STAT3 protein. Taken together, these data show that propofol inhibits miR-17 expression and further alleviates vascular endothelial cell injury during ischemia-reperfusion by reducing apoptosis of vascular endothelial cells in vitro.