ArticleMolecular and cellular biochemistry2022
Blueberry extract attenuates norepinephrine-induced oxidative stress and apoptosis in H9c2 cardiac cells.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Targeting FOXO3 for the Management of Heart Failure: Current Evidence and Future Directions.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Wild blueberry-derived polyphenol metabolites attenuate telomere shortening in an in vitro model of metabolic syndrome.European journal of nutrition · 2026Article
- Tyrosine hydroxylase as a therapeutic target: insights from adrenergic nerve and TNBC cell interactions.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Investigating the Role of Autonomic Dysfunction in the Pathogenesis of Depression-Related Dry Eye.Translational vision science & technology · 2025Article
- Sympathetic overactivation and catecholamine toxicity: mechanisms and therapeutic strategies for neurogenic heart injury following acute ischemic stroke.Frontiers in cardiovascular medicine · 2025Review
- Article
- Impact of blueberry extract on hematological response in phenylhydrazine-induced hemolytic anemia.Hematology, transfusion and cell therapyArticle
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
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Abstract
Enhanced sympathetic system activation mediated by norepinephrine (NE) contributes to adverse cardiac remodeling leading to oxidative stress and cell death, progressing to heart failure. Natural antioxidants may help maintain redox balance, attenuating NE-mediated cardiac cell damage. In the present study, we evaluated the effect of a blueberry extract (BBE) on H9c2 cardiac cells exposed to NE on cell death, oxidative stress status and its major signaling pathways. H9c2 cells were pre-incubated with 50 μg/ml of BBE for 4 h and maintained in the presence of 100 μM NE for 24 h. NE exposure resulted in increased caspase 3/7 activity. This was associated with reduced protein expression of antioxidants catalase, superoxide dismutase and glutathione peroxidase and increase in 4-hydroxynonenal adduct formation. NE led to increased activity of Protein kinase B (Akt), Forkhead box O3a and AMP-activated protein kinase alpha and decreased activity of Signal transducer and activator of transcription 3. BBE prevented caspases activation and abrogated NE-induced increase in oxidative stress, as well as attenuated the increase in Akt. Based on these findings, it is concluded that BBE promoted cardioprotection of H9c2 cells in an in vitro model of NE-induced oxidative damage, suggesting a cardioprotective role for BBE in response to NE exposure.
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