Broccoli sprout extract prevents diabetic cardiomyopathy via Nrf2 activation in db/db T2DM mice
Xu Z, Wang S, Ji H, Zhang Z, Chen J, Tan Y, Wintergerst K, Zheng Y, Sun J, Cai L
Scientific reports · 66 citas
Cómo se estudió
- Diseño
- Estudio en animales (clasificado por nuestro filtro de IA)
- Estudiado en
- Animales
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación independiente
- Organización sin fines de lucro
- American Diabetes Association
- Gobierno
- National Natural Science Foundation of China
- Gobierno
- People's Government of Jilin Province
- Subvenciones
- National Natural Science Foundation of China (81270293); National Natural Science Foundation of China (1-15-BS-018); National Natural Science Foundation of China (81570339); American Diabetes Association (81570338); National Natural Science Foundation of China (81370318); American Diabetes Association (81270293); American Diabetes Association (1–15-BS-018); American Diabetes Association (1-13-JF-53); National Natural Science Foundation of China (81570338); American Diabetes Association (81370318); National Natural Science Foundation of China (1-13-JF-53)
Según 3 financiadores declarados y la declaración de financiación del texto completo.
Publicación
- Publicado
- 2016-07-26 · Sci Rep · vol. 6 · número 1 · pág. 30252
- Editorial
- Nature Portfolio
- Citado
- 87 citas · más que el 97% de estudios similares · 6.2× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 53 trabajos
- Acceso
- Acceso abierto (revista) · CC-BY
- Áreas de investigación
- Genomics, phytochemicals, and oxidative stress · Coenzyme Q10 studies and effects · Adipose Tissue and Metabolism
- Palabras clave
- Diabetic cardiomyopathy, Cardiomyopathy, Medicine, Internal medicine, Pharmacology, Endocrinology, Chemistry, Cardiology, Heart failure
- MeSH
- animals, mice, inbred nod, humans, mice, brassica, diabetes mellitus, type 2, disease models, animal, isothiocyanates, sulfoxides, plant extracts, gene expression regulation, oxidation-reduction, oxidative stress, nf-e2-related factor 2, diabetic cardiomyopathies
10 autores
- Zheng Xu🇺🇸🇨🇳University of Louisville; Jilin University; Kosair Children's Hospital; First Hospital of Jilin University
- Shudong Wang🇺🇸🇨🇳University of Louisville; Jilin University; Kosair Children's Hospital; First Hospital of Jilin University
- Honglei Ji🇨🇳Jilin University; First Hospital of Jilin University
- Zhiguo Zhang🇨🇳Jilin University; First Hospital of Jilin University
- Jing Chen🇺🇸University of Louisville; Kosair Children's Hospital
- Yi Tan🇺🇸University of Louisville; Kosair Children's Hospital; Diabetes Care Center
- Kupper A. Wintergerst🇺🇸University of Louisville; Diabetes Care Center
- Yang Zheng🇨🇳Jilin University; First Hospital of Jilin University
- Jian Sun🇨🇳Jilin University; First Hospital of Jilin University
- Lu Cai🇺🇸University of Louisville; Kosair Children's Hospital; Diabetes Care Center
Resumen
El texto original del estudio, en el idioma en que se publicó.
To develop a clinic-relevant protocol for systemic up-regulation of NFE2-related factor 2 (Nrf2) to prevent diabetic cardiomyopathy (DCM), male db/db and age-matched wild-type (WT) mice were given sulforaphane (SFN, an Nrf2 activator) and its natural source, broccoli sprout extract (BSE) by gavage every other day for 3 months, with four groups: vehicle (0.1 ml/10 g), BSE-low dose (estimated SFN availability at 0.5 mg/kg), BSE-high dose (estimated SFN availability at 1.0 mg/kg), and SFN (0.5 mg/kg). Cardiac function and pathological changes (hypertrophy, fibrosis, inflammation and oxidative damage) were assessed by echocardiography and histopathological examination along with Western blot and real-time PCR, respectively. Both BSE and SFN significantly prevented diabetes-induced cardiac dysfunction, hypertrophy and fibrosis. Mechanistically, BSE, like SFN, significantly up-regulated Nrf2 transcriptional activity, evidenced by the increased Nrf2 nuclear accumulation and its downstream gene expression. This resulted in a significant prevention of cardiac oxidative damage and inflammation. For all these preventive effects, BSE at high dose provided a similar effect as did SFN. These results indicated that BSE at high dose prevents DCM in a manner congruent with SFN treatment. Therefore, it suggests that BSE could potentially be used as a natural and safe treatment against DCM via Nrf2 activation.
Resumen vía Europe PMC. Los derechos de autor siguen siendo de los autores o la editorial (CC BY).
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