UCP2 silencing blocks the mifepristone-mediated UCP2 induction and antioxidant effects.

<p><b>A-H:</b> b.End3 microvascular endothelial cells were transfected with UCP2 siRNA or negative control siRNA and exposed to high glucose for 5 days. Subsequently the cells were treated with mifepristone (3 μM) for 1 day. <b>A</b>: The mitochondrial superoxide production was measured by MitoSOX Red. <b>B</b>: The cellular H₂O₂ production was measured by CM-H₂DCFDA. <b>C, D</b>: The mitochondrial membrane potential was measured by JC-1 (<b>C</b>) and also by the uptake of MitoTracker Green (<b>D</b>). <b>E</b>: The cellular viability was determined by measuring the Hoechst 33342 DNA dye uptake. <b>F</b>: The cellular ATP content was measured. <b>G</b>: The viability was determined by measuring the Hoechst 33342 DNA dye uptake. <b>H:</b> Cellular ATP content was determined. (#p<0.05 high-glucose exposure induced significant changes compared to cells maintained in low glucose containing medium,*p<0.05 UCP2 silencing induced significant changes in ROS production and in the mitochondrial potential, § p<0.05 mifepristone significantly reduced the ROS production and the mitochondrial potential.)