RGD Reference Report - Prevention by sulforaphane of diabetic cardiomyopathy is associated with up-regulation of Nrf2 expression and transcription activation. - Rat Genome Database

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Prevention by sulforaphane of diabetic cardiomyopathy is associated with up-regulation of Nrf2 expression and transcription activation.

Authors: Bai, Y  Cui, W  Xin, Y  Miao, X  Barati, MT  Zhang, C  Chen, Q  Tan, Y  Cui, T  Zheng, Y  Cai, L 
Citation: Bai Y, etal., J Mol Cell Cardiol. 2013 Apr;57:82-95. doi: 10.1016/j.yjmcc.2013.01.008. Epub 2013 Jan 23.
RGD ID: 10412721
Pubmed: PMID:23353773   (View Abstract at PubMed)
DOI: DOI:10.1016/j.yjmcc.2013.01.008   (Journal Full-text)

This study was to investigate whether sulforaphane (SFN) can prevent diabetic cardiomyopathy. Type 1 diabetes was induced in FVB mice by multiple intraperitoneal injections with low-dose streptozotocin. Hyperglycemic and age-matched control mice were treated with or without SFN at 0.5mg/kg daily in five days of each week for 3 months and then kept until 6 months. At 3 and 6 months of diabetes, blood pressure and cardiac function were assessed. Cardiac fibrosis, inflammation, and oxidative damage were assessed by Western blot, real-time qPCR, and histopathological examination. SFN significantly prevented diabetes-induced high blood pressure and cardiac dysfunction at both 3 and 6 months, and also prevented diabetes-induced cardiac hypertrophy (increased the ratio of heart weight to tibia length and the expression of atrial natriuretic peptide mRNA and protein) and fibrosis (increased the accumulation of collagen and expression of connective tissue growth factor and tissue growth factor-beta). SFN also almost completely prevented diabetes-induced cardiac oxidative damage (increased accumulation of 3-nitrotyrosine and 4-hydroxynonenal) and inflammation (increased tumor necrotic factor-alpha and plasminogen activator inhibitor 1 expression). SFN up-regulated NFE2-related factor 2 (Nrf2) expression and transcription activity that was reflected by increased Nrf2 nuclear accumulation and phosphorylation as well as the mRNA and protein expression of Nrf2 downstream antioxidants. Furthermore, in cultured H9c2 cardiac cells silencing Nrf2 gene with its siRNA abolished the SFN's prevention of high glucose-induced fibrotic response. These results suggest that diabetes-induced cardiomyopathy can be prevented by SFN, which was associated with the up-regulated Nrf2 expression and transcription function.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
NFE2L2HumanDiabetic Cardiomyopathies treatmentISONfe2l2 (Mus musculus)associated with Diabetes Mellitus and ExperimentalRGD 
Nfe2l2RatDiabetic Cardiomyopathies treatmentISONfe2l2 (Mus musculus)associated with Diabetes Mellitus and ExperimentalRGD 
Nfe2l2MouseDiabetic Cardiomyopathies treatmentIEP associated with Diabetes Mellitus and ExperimentalRGD 

Objects Annotated

Genes (Rattus norvegicus)
Nfe2l2  (NFE2 like bZIP transcription factor 2)

Genes (Mus musculus)
Nfe2l2  (nuclear factor, erythroid derived 2, like 2)

Genes (Homo sapiens)
NFE2L2  (NFE2 like bZIP transcription factor 2)


Additional Information