Research Paper Volume 10, Issue 7 pp 1722—1744

Heme oxygenase-1 ameliorates oxidative stress-induced endothelial senescence via regulating endothelial nitric oxide synthase activation and coupling

Figure 6. HO-1 protected the coupling state of eNOS in endothelial senescence. (A) HO-1 inducer Hemin increased the downregulation of dimer/monomer-eNOS ratio stimulated by H2O2. *P < 0.05 vs. Control; and #P < 0.05 vs. H2O2. n = 6. (B) Overexpression of HO-1 infected by recombinant adenovirus increased the downregulation of dimer/monomer-eNOS ratio stimulated by H2O2. *P < 0.05 vs. Ad-GFP; and #P < 0.05 vs. Ad-GFP+H2O2. n = 3. (C) Silencing of HO-1 decreased the dimer/monomer-eNOS ratio. *P < 0.05 vs. Control or NC-siRNA. n = 5. (D, E and F) Images of DHE fluorescence staining taken by confocal microscopy showing ROS production in HUVECs (200 × magnification). The fluorescence intensity of DHE was normalized to the cell numbers by normalizing to DAPI fluorescence (not shown). (D) treated with or without H2O2 and Hemin. *P < 0.05 vs. Control; and #P < 0.05 vs. H2O2. n = 4. (E) infected with or without HO-1 recombinant adenovirus. *P < 0.05 vs. Ad-GFP; and #P < 0.05 vs. Ad-GFP+H2O2. n = 6. (F) transfected with or without HO-1 siRNA. *P < 0.05 vs. Control or NC-siRNA. n = 6.