作者: Jie Li , Junfeng Li , Tingting Wei , Junhua Li
DOI: 10.1159/000447795
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摘要: Background/Aims: To investigate the effects of miR-137 on high glucose (HG)-induced vascular injury, and to establish mechanism underlying these effects. Methods: Human umbilical vein endothelial cells (HUVECs) were transfected with inhibitor or mimic, then treated normal glucose. Cell viability apoptosis detected by using Counting Kit-8 (CCK-8) assay flow cytometry, respectively. Reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) fluorescent probe (DCFH-DA), thiobarbituric acid reaction, nitroblue tetrazolium assay, The mRNA protein expressions AMPKα1 determined qRT-PCR Western blotting. Results: Down-regulation dramatically reverted HG-induced decreases in cell SOD levels increases apoptosis, ROS MDA levels. Moreover, bioinformatics analysis predicted that was a potential target gene miR-137. Luciferase reporter demonstrated could directly AMPKα1. overexpression had similar effect as inhibition. HUVECs partially reversed protective inhibition oxidative stress HUVECs. Conclusion: ameliorates injury AMPKα1, leading increasing cellular reductive reactions decreasing stress. These results provide further evidence for injury.