Sulforaphane prevention of diabetes-induced aortic damage was associated with the up-regulation of Nrf2 and its down-stream antioxidants
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- 作者：Xiao Miao (1) (2)
Yang Bai (2) (3)
Weixia Sun (2) (4)
Wenpeng Cui (1) (2)
Ying Xin (2) (5)
Yuehui Wang (1)
Yi Tan (2) (6)
Lining Miao (1)
Yaowen Fu (4)
Guanfang Su (1)
Lu Cai (2) (6) (7) - 关键词：Sulforaphane ; Nrf2 ; aorta ; Oxidative damage ; Vascular inflammation
- 刊名：Nutrition & Metabolism
- 出版年：2012
- 出版时间：December 2012
- 年：2012
- 卷：9
- 期：1
- 全文大小：542KB
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Yang Bai (2) (3)
Weixia Sun (2) (4)
Wenpeng Cui (1) (2)
Ying Xin (2) (5)
Yuehui Wang (1)
Yi Tan (2) (6)
Lining Miao (1)
Yaowen Fu (4)
Guanfang Su (1)
Lu Cai (2) (6) (7)
1. The Second Hospital of Jilin University, Changchun, China
2. KCHRI at the Department of Pediatrics, University of Louisville, Louisville, USA
3. The People’s Hospital of Jilin Province, Changchun, China
4. The First Hospital of Jilin University, Changchun, China
5. Normal Bethune Medical College of Jilin University, Changchun, China
6. Chinese-American Research Institute for Diabetic Complications at Wenzhou Medical College, Wenzhou, China
7. Departments of Radiation Oncology and Pharmacology and Toxicology, The University of Louisville, Louisville, USA - ISSN：1743-7075
文摘
Background Oxidative stress plays an important role in diabetes-induced vascular inflammation and pathogenesis. Nuclear factor E2-related factor-2 (Nrf2) is a transcription factor orchestrating antioxidant and cyto-protective responses to oxidative stress. In the present study, we tested whether sulforaphane (SFN) can protect the aorta from diabetes and, if so, whether the aortic protection is associated with up-regulation of Nrf2 and its down-stream antioxidants. Methods Type 1 diabetes was induced in FVB mice by multiple low-dose streptozotocin. Diabetic and age-matched control mice were treated with or without SFN at 0.5?mg/kg daily in five days of each week for three months. At the end of 3?months treatment of SFN one set of mice were sacrificed to perform the experimental measurements. The second set of both diabetic and control mice were aged for additional 3?months without further SFN treatment and then sacrificed to perform the experimental measurements. Aortas from these mice were assessed for fibrosis, inflammation, oxidative damage, and Nrf2 expression and transcription by immunohistochemical staining and real-time PCR method, respectively. Results Diabetes induced significant increases in oxidative stress and inflammation in the aorta at both 3 and 6?months, and fibrotic response at 6?months. SFN completely prevented these diabetic pathogenic changes and also significantly up-regulated the expression of Nrf2 and its down-stream antioxidants. Conclusions These results suggest that diabetes-induced aortic fibrosis, inflammation, and oxidative damage can be prevented by SFN. The aortic protection from diabetes by SFN was associated with the up-regulation of Nrf2 and its downstream antioxidants.