Blueberry extract attenuates norepinephrine-induced oxidative stress and apoptosis in H9c2 cardiac cells

• Published in: Molecular and cellular biochemistry Vol. 477; no. 3; pp. 663 - 672
• Main Authors: Türck, Patrick, Nemec-Bakk, Ashley, Talwar, Tanu, Suntres, Zacharias, Belló-Klein, Adriane, da Rosa Araujo, Alex Sander, Khaper, Neelam
• Format: Journal Article
• Language: English
• Published: New York Springer US 01-03-2022; Springer; Springer Nature B.V
• Subjects: 4-Hydroxynonenal; AKT protein; AMP-activated protein kinase; Animals; Antioxidants; Apoptosis; Apoptosis - drug effects; Attenuation; Biochemistry; Biomedical and Life Sciences; Blueberry Plants - chemistry; Cardiology; Caspase-3; Catalase; Catecholamines; Cell activation; Cell death; Cell Line; Congestive heart failure; Damage; Exposure; Forkhead protein; Glutathione; Glutathione peroxidase; Heart cells; Kinases; Life Sciences; Medical Biochemistry; Myoblasts, Cardiac - metabolism; Norepinephrine; Norepinephrine - pharmacology; Oncology; Oxidative stress; Oxidative Stress - drug effects; Peroxidase; Plant Extracts - chemistry; Plant Extracts - pharmacology; Protein kinases; Proteins; Rats; Superoxide; Superoxide dismutase; Transcription; H9c2; Norepinephrine; Cardiac remodeling; Redox signaling; Blueberry
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-021-04313-z

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.