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Oxidative Medicine and Cellular Longevity
Volume 2012, Article ID 542042, 7 pages
Research Article

Sodium-Glucose Cotransporter Inhibition Prevents Oxidative Stress in the Kidney of Diabetic Rats

1Renal Pathophysiology Laboratory, Department of Nephrology, Instituto Nacional de Cardiología “Ignacio Chávez”, Juan Badiano 1, 14080 Mexico City, DF, Mexico
2Health Science Faculty, Universidad Anáhuac, México Norte, 57286 Huixquilucan, State of Mexico, Mexico
3Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV), 07360 Mexico City, Mexico
4Department of Molecular Biomedicine, CINVESTAV-Monterrey, 66600 Apodaca, NL, Mexico

Received 7 June 2012; Accepted 13 October 2012

Academic Editor: José Luis Martín-Ventura

Copyright © 2012 Horacio Osorio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.