Heme oxygenase-1 prevents superoxide anion-associated endothelial cell sloughing in diabetic rats.
Biochem Biophys Res Commun
; 315(2): 509-16, 2004 Mar 05.
Article
en En
| MEDLINE
| ID: mdl-14766238
ABSTRACT
Heme oxygenase-1 (HO-1) represents a key defense mechanism against oxidative injury. Hyperglycemia has been linked to increased oxidative stress, leading to endothelial dysfunction, delayed cell replication, and enhanced apoptosis. The effect of streptozotocin (STZ)-induced diabetes on HO activity, HO-1 promoter activity, superoxide anion (O*-2, and the number of circulating endothelial cells was measured. The expression of HO-1/HO-2 protein was unchanged, but HO activity was decreased in aortas of diabetic rats compared with control (p < 0.05). High glucose decreased HO-1 promoter activity (p < 0.05). Hyperglycemia increased O*-2 and this increase was augmented with HO-1 inhibition and diminished with HO-1 upregulation (p < 0.05). Circulating endothelial cells were significantly higher in diabetic rats and were decreased or increased with administration of the HO-1 inducer (CoPP) or inhibitor (SnMP), respectively (p<0.05). In conclusion, HO-1 upregulation in diabetic rats brings about an increase in serum bilirubin, a reduction in O*-2 production, and a decrease in endothelial cell sloughing.
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Base de datos:
MEDLINE
Asunto principal:
Células Endoteliales
/
Hemo Oxigenasa (Desciclizante)
Tipo de estudio:
Risk_factors_studies
Idioma:
En
Revista:
Biochem Biophys Res Commun
Año:
2004
Tipo del documento:
Article