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Oxidative Medicine and Cellular Longevity
Volume 2012, Article ID 821936, 12 pages
Research Article

Prevention of Diabetic Nephropathy by Sulforaphane: Possible Role of Nrf2 Upregulation and Activation

1Department of Nephrology, The Second Hospital Jilin University, 218 Ziqiang Street, Changchun 130041, China
2Department of Pediatrics, University of Louisville, 570 South Preston Street, Baxter I, Suite 304F, Louisville, KY 40202, USA
3The People’s Hospital of Jilin Province, Changchun, China
4Department of Ophthalmology, The Second Hospital Jilin University, Changchun, China
5School of Public Health Jilin University, Changchun, China
6Chinese-American Research Institute for Diabetic Complications, Wenzhou Medical College, Wenzhou, China
7Department of Medicine, University of Louisville, Louisville, KY, USA
8Departments of Radiation Oncology and Pharmacology & Toxicology, University of Louisville, Louisville, KY, USA

Received 17 July 2012; Revised 18 August 2012; Accepted 23 August 2012

Academic Editor: Jingbo Pi

Copyright © 2012 Wenpeng Cui 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 present study was to investigate whether sulforaphane (SFN) can prevent diabetic nephropathy in type 1 diabetic mouse model induced by multiple low-dose streptozotocin. Diabetic and age-matched control mice were given SFN at 0.5 mg/kg body weight daily for 3 months. At the end of 3-month SFN treatment, the diabetic nephropathy, shown by renal inflammation, oxidative damage, fibrosis, and dysfunction, was significantly prevented along with an elevation of renal Nrf2 expression and transcription in diabetes/SFN group compared with diabetic group. However, this renal prevention by SFN was not seen when the 3-month SFN-treated diabetic mice were aged for additional 3 months without further SFN treatment. Nrf2-mediated renal protective effects in diabetes were evaluated in human renal tubular HK11 cells transfected with control and Nrf2 siRNA and treated with 27.5 mM mannitol or high glucose plus palmitate (300 μM). Blockade of Nrf2 expression completely abolished SFN prevention of the profibrotic effect induced by high glucose plus palmitate. These results support that renal Nrf2 expression and its transcription play important roles in SFN prevention of diabetes-induced renal damage. However, the SFN preventive effect on diabetes-induced renal pathogeneses is not sustained, suggesting the requirement of continual use of SFN for its sustained effect.