Coenzyme Q10 Attenuates High Glucose-Induced Endothelial Progenitor Cell Dysfunction through AMP-Activated Protein Kinase Pathways

Figure 5

CoQ10 improves high glucose-induced EPCs dysfunction by upregulation of eNOS and HO-1. Cells were cultured with comp C (20 μM), L-NAMEA (100 μM), and SnPP IX (10 μM) for 60 min before CoQ10 incubation under high glucose conditions. (a) EPC migration was measured by Boyden chamber assay. The migrated cells were stained with fluorescein isothiocyanate UEA-1 (lectin) (green) and counted under the fluorescence microscope. (b) Mitochondrial apoptosis was detected by JC-1. Loss of mitochondrial membrane potential () was assessed by the change in JC-1-derived fluorescence from red to green. The ratio of red/green fluorescence represented in EPCs. (c) ROS production of EPCs was assessed by staining with DCFH-DA. (d) The mitochondrial function was measured using Rh123 dye (5 mM), and the fluorescence intensity was measured at 485-nm excitation and 530-nm emission using a fluorescent microplate reader. (e) Expressions of activated-caspase 3 and Bcl2 protein were assessed by western blot. (f) Cells were transfected with scramble and HO-1 siRNA (10 nM), respectively, in CoQ10-treated EPCs under high glucose conditions, and the expressions of activated-caspase 3 and HO-1 protein were detected by western blot. Comp C: component C, AMPK inhibitor; L-NAME, NO inhibitor; Snpp IX, HO-1 inhibitor. Data are mean ± SE; ; versus control (5 mM glucose); versus high glucose (HG); versus HG-CoQ10.

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