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 1. Induction or overexpression of HO-1 reversed HUVEC senescence. (A) Upregulation of HO-1 protein expression in HUVEC induced by Hemin or transfected with HO-1 recombinant adenovirus (HO-1, 32kDa; GFP-HO-1, 59kDa). *P < 0.05 vs. Control; #P < 0.05 vs. Ad-GFP. n = 5. (B) HUVEC were stained for SA-β-galactosidase treated with H2O2 (50 μM, 1 h) or/and Hemin (0.1-10 μM). Senescent cells appeared blue (200 × magnification). *P < 0.05 vs. Control; #P < 0.05 vs. H2O2. n = 5. (C) SA-β-gal staining of HUVEC treated with H2O2 (50 μM, 1 h) or/and HO-1 recombinant adenovirus (200 × magnification). *P < 0.05 vs. Control; #P < 0.05 vs. Ad-GFP+H2O2. n = 5. (D) Hemin attenuated the expression of p53 or p21 stimulated by H2O2. *P < 0.05 vs. Control; #P < 0.05 vs. H2O2. n = 5. (E) Overexpression of HO-1 infected by recombinant adenovirus decreased the upregulation of p53 or p21 stimulated by H2O2. *P < 0.05 vs. Ad-GFP; #P < 0.05 vs. Ad-GFP+H2O2. n = 5. (F) Hemin attenuated the expression of γH2A.X (Ser139) stimulated by H2O2. *P < 0.05 vs. Control; and #P < 0.05 vs. H2O2. n = 5.