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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 4693801, 11 pages
http://dx.doi.org/10.1155/2016/4693801
Research Article

Anti-Inflammatory Therapy Modulates Nrf2-Keap1 in Kidney from Rats with Diabetes

1Laboratory of Renal Physiopathology, Juan Badiano 1, 14080 Mexico City, DF, Mexico
2Department of Nephrology, Instituto Nacional de Cardiología-Ignacio Chávez, Juan Badiano 1, 14080 Mexico City, DF, Mexico
3Histopathology Laboratory, Research Subdivision, School of Medicine, Universidad Panamericana, Donatello 43, 03910 Mexico City, DF, Mexico

Received 10 November 2015; Revised 18 December 2015; Accepted 3 January 2016

Academic Editor: Silvana Hrelia

Copyright © 2016 Abraham Said Arellano-Buendía 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.

Abstract

This study addressed the relationship of proinflammatory cytokines and Nrf2-Keap1 system in diabetic nephropathy. The experimental groups were control, diabetic, and diabetic treated with mycophenolate mofetil (MMF). The renal function, proinflammatory and profibrotic cytokines, oxidative stress, morphology, and nephrin expression were assessed. Diabetic group showed impaired renal function in association with oxidative stress and decreased Nrf2 nuclear translocation. These results were associated with increased mesangial matrix index, interstitial fibrosis, and increased nephrin expression in cortex and urine excretion. Additionally, interleukin-1β, IL-6, and transforming growth factor-β1 were increased in plasma and kidney. MMF treatment conserved renal function, prevented renal structural alterations, and partially prevented the proinflammatory and profibrotic cytokines overexpression. Despite that MMF treatment induced nephrin overexpression in renal tissue, preventing its urinary loss. MMF salutary effects were associated with a partial prevention of oxidative stress, increased Nrf2 nuclear translocation, and conservation of antioxidant enzymes in renal tissue. In conclusion, our results confirm that inflammation is a key factor in the progression of diabetic nephropathy and suggest that treatment with MMF protects the kidney by an antioxidant mechanism, possibly regulated at least in part by the Nrf2/Keap1 system, in addition to its well-known anti-inflammatory effects.