ArticleHerz2014
Sulforaphane protects H9c2 cardiomyocytes from angiotensin II-induced hypertrophy.
Article in Herz, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- Empagliflozin inhibits angiotensin II-induced hypertrophy in H9c2 cardiomyoblasts through inhibition of NHE1 expression.Molecular and cellular biochemistry · 2022Article
- Predictive value and regulatory mechanism of serum miR-499a-5p on myocardial dysfunction in sepsis.Journal of cardiothoracic surgery · 2021Article
- Aliskiren attenuates cardiac dysfunction by modulation of the mTOR and apoptosis pathways.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2020Article
- Effect of sulphoraphane on newborn mouse cardiomyocytes undergoing ischaemia/reperfusion injury.Pharmaceutical biology · 2019Article
- Effects of the isothiocyanate sulforaphane on TGF-β1-induced rat cardiac fibroblast activation and extracellular matrix interactions.Journal of cellular physiology · 2019Article
- Neutrophil Gelatinase-Associated Lipocalin2 Exaggerates Cardiomyocyte Hypoxia Injury by Inhibiting Integrin β3 Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- The Glp-1 Analog Liraglutide Protects Against Angiotensin II and Pressure Overload-Induced Cardiac Hypertrophy via PI3K/Akt1 and AMPKa Signaling.Frontiers in pharmacology · 2019Article
- Review
- Analysis of microRNA Expression Profiles Induced by Yiqifumai Injection in Rats with Chronic Heart Failure.Frontiers in physiology · 2018Article
- Article
- Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress.Acta pharmacologica Sinica · 2016Article
- Modulation of apoptosis by sulforaphane is associated with PGC-1α stimulation and decreased oxidative stress in cardiac myoblasts.Molecular and cellular biochemistry · 2015Article
- Mitochondrial permeability transition triggers the release of mtDNA fragments.Cellular and molecular life sciences : CMLS · 2004Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiac hypertrophy is an adaptive process of the heart in response to various stimuli, but sustained cardiac hypertrophy will finally lead to heart failure. Sulforaphane-extracted from cruciferous vegetables of the genus Brassica such as broccoli, brussels sprouts, and cabbage-has been evaluated for its anticarcinogenic and antioxidant effects.
aimsTo investigate the effect of sulforaphane on angiotensin II (Ang II)-induced cardiac hypertrophy in vitro.
methodsEmbryonic rat heart-derived H9c2 cells were co-incubated with sulforaphane and Ang II. The cell surface area and mRNA levels of hypertrophic markers were measured to clarify the effect of sulforaphane on cardiac hypertrophy. The underlying mechanism was further investigated by detecting the activation of Akt and NF-κB signaling pathways.
resultsWe found that H9c2 cells pretreated with sulforaphane were protected from Ang II-induced hypertrophy. The increasing mRNA levels of ANP, BNP, and β-MHC in Ang II-stimulated cells were also down-regulated after sulforaphane treatment. Moreover, sulforaphane repressed the Ang II-induced phosphorylation of Akt, GSK3β, mTOR, eIF4e, as well as of IκBα and NF-κB.
conclusionBased on our results, sulforaphane attenuates Ang II-induced hypertrophy of H9c2 cardiomyocytes mediated by the inhibition of intracellular signaling pathways including Akt and NF-κB.
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