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Oxidative Medicine and Cellular Longevity
Volume 2014, Article ID 123963, 11 pages
Research Article

Sulforaphane Attenuation of Type 2 Diabetes-Induced Aortic Damage Was Associated with the Upregulation of Nrf2 Expression and Function

1Cardiovascular Center at the First Hospital of Jilin University, 71 Xinmin Street, Changchun 130021, China
2Kosair Children’s Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA
3The Chinese-American Research Institute, Wenzhou Medical University, Wenzhou 325035, China
4Departments of Radiation Oncology, Pharmacology and Toxicology, University of Louisville, Louisville, KY 40292, USA

Received 3 November 2013; Revised 11 December 2013; Accepted 6 January 2014; Published 23 February 2014

Academic Editor: Adriane Belló-Klein

Copyright © 2014 Yonggang Wang 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.


Type 2 diabetes mellitus (T2DM) significantly increases risk for vascular complications. Diabetes-induced aorta pathological changes are predominantly attributed to oxidative stress. Nuclear factor E2-related factor-2 (Nrf2) is a transcription factor orchestrating antioxidant and cytoprotective responses to oxidative stress. Sulforaphane protects against oxidative damage by increasing Nrf2 expression and its downstream target genes. Here we explored the protective effect of sulforaphane on T2DM-induced aortic pathogenic changes in C57BL/6J mice which were fed with high-fat diet for 3 months, followed by a treatment with streptozotocin at 100 mg/kg body weight. Diabetic and nondiabetic mice were randomly divided into groups with and without 4-month sulforaphane treatment. Aorta of T2DM mice exhibited significant increases in the wall thickness and structural derangement, along with significant increases in fibrosis (connective tissue growth factor and transforming growth factor), inflammation (tumor necrosis factor-α and vascular cell adhesion molecule 1), oxidative/nitrative stress (3-nitrotyrosine and 4-hydroxy-2-nonenal), apoptosis, and cell proliferation. However, these pathological changes were significantly attenuated by sulforaphane treatment that was associated with a significant upregulation of Nrf2 expression and function. These results suggest that sulforaphane is able to upregulate aortic Nrf2 expression and function and to protect the aorta from T2DM-induced pathological changes.