Glucocorticoids Suppress Mitochondrial Oxidant Production via Upregulation of Uncoupling Protein 2 in Hyperglycemic Endothelial Cells
Fig 3
Mifepristone inhibits the glucose-induced mitochondrial ROS production in microvascular endothelial cells.
A-D: b.End3 microvascular endothelial cells were exposed to high glucose for 7 days and were treated with dexamethasone and mifepristone (A, B) or with mifepristone alone (C, D) at the indicated concentrations for 3 days. A, C: The ROS production was measured with the mitochondrial superoxide specific MitoSOX Red B, D: The viability was determined by measuring the Hoechst 33342 DNA dye uptake. E, F: bEnd.3 BALB/c murine microvascular endothelial cells were exposed to high glucose for 7 days and were treated with mifepristone for 3 days at the indicate concentrations. E: The mitochondrial ROS production was measured by MitoSOX Red and F: the viability was determined by the Hoechst 33342 uptake. (#p<0.05 high-glucose exposure induced significant changes compared to cells maintained in low glucose containing medium,*p<0.05 glucocorticoid treatment significantly reduced the ROS production, §p<0.05 mifepristone induced significant reduction in the ROS generation compared to dexamethasone alone.)