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Oxid Med Cell Longev. 2012;2012:542042. doi: 10.1155/2012/542042. Epub 2012 Nov 20.

Sodium-glucose cotransporter inhibition prevents oxidative stress in the kidney of diabetic rats.

Author information

1
Renal Pathophysiology Laboratory, Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano 1, 14080 Mexico City, DF, Mexico. horace_33@yahoo.com.mx

Abstract

The hyperglycemia triggers several chronic diabetic complications mediated by increased oxidative stress that eventually causes diabetic nephropathy. The aim of this study was to examine if the sodium-glucose cotransporter (SGLT2) inhibition prevents the oxidative stress in the kidney of diabetic rats.

METHODS:

The diabetic rat model was established by intraperitoneal injection of streptozotocin (50 mg/kg). The inhibition of SGLT2 was induced by daily subcutaneous administration of phlorizin (0.4 g/kg). Oxidative stress was assessed by catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities and by immunohistochemical analysis of 3-nitrotyrosine (3-NT).

RESULTS:

Streptozotocin-induced diabetes caused hyperglycemia and lower body weight. The CAT activity decreased in cortex and medulla from diabetic rats; in contrast, the GPx activity increased. Furthermore the 3-NT staining of kidney from diabetic rats increased compared to control rats. The inhibition of SGLT2 decreased hyperglycemia. However, significant diuresis and glucosuria remain in diabetic rats. The phlorizin treatment restores the CAT and GPX activities and decreases 3-NT staining.

CONCLUSION:

The inhibition of SGLT2 by phlorizin prevents the hyperglycemia and oxidative stress in kidney of diabetic rats, suggesting a prooxidative mechanism related to SGLT2 activity.

PMID:
23227274
PMCID:
PMC3512343
DOI:
10.1155/2012/542042
[Indexed for MEDLINE]
Free PMC Article
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