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J Cell Mol Med. 2019 Jul 3. doi: 10.1111/jcmm.14520. [Epub ahead of print]

Protection against diabetic cardiomyopathy is achieved using a combination of sulforaphane and zinc in type 1 diabetic OVE26 mice.

Author information

1
The Center of Cardiovascular Diseases, The First Hospital of Jilin University, Changchun, China.
2
Pediatric Research Institute, Department of Pediatrics, University of Louisville, Louisville, Kentucky, USA.
3
Department of Nephrology, The First Hospital of Jilin University, Changchun, China.
4
Department of Otolaryngology, Stanford University, Palo Alto, California, USA.
5
Department of Bioinformatics and Biostatistics, University of Louisville, Louisville, Kentucky, USA.
6
Departments of Radiation Oncology, Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky, USA.

Abstract

Sulforaphane (SFN) can effectively induce nuclear factor E2-related factor 2 (Nrf2), and zinc (Zn) can effectively induce metallothionein (MT), both of which have been shown to protect against diabetic cardiomyopathy (DCM). However, it is unclear whether combined treatment with SFN and Zn offers better cardiac protection than either one alone. Here, we treated 5-week-old OVE mice that spontaneously develop type 1 diabetes with SFN and/or Zn for 18 weeks. Cardiac dysfunction, by echocardiography, and pathological alterations and remodelling, shown by cardiac hypertrophy, fibrosis, inflammation and oxidative damage, examined by histopathology, Western blotting and real-time PCR, were observed in OVE mice. All these dysfunction and pathological abnormalities seen in OVE mice were attenuated in OVE mice with treatment of either SFN, Zn or SFN/Zn, and the combined treatment with SFN/Zn was better than single treatments at ameliorating DCM. In addition, combined SFN and Zn treatment increased Nrf2 function and MT expression in the heart of OVE mice to a greater extent than SFN or Zn alone. This indicates that the dual activation of Nrf2 and MT by combined treatment with SFN and Zn may be more effective than monotherapy at preventing the development of DCM via complementary, additive mechanisms.

KEYWORDS:

cardiomyopathy; diabetes; metallothionein; nuclear factor E2; related factor 2; sulforaphane; zinc

PMID:
31270951
DOI:
10.1111/jcmm.14520
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