Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage
Dyslipidemia is a prominent pathological feature responsible for oxidative stress-induced cardiac damage. Due to their high antioxidant content, dietary compounds, such as aspalathin and sulforaphane, are increasingly explored for their cardioprotective effects against lipid-induced toxicity. Cultur...
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| Format: | Article |
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Elsevier
2025-03-01
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| Series: | Metabolism Open |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2589936825000027 |
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| author | Sinenhlanhla X.H. Mthembu Sithandiwe E. Mazibuko-Mbeje Sonia Silvestri Patrick Orlando Bongani B. Nkambule Christo J.F. Muller Luca Tiano Phiwayinkosi V. Dludla |
| author_facet | Sinenhlanhla X.H. Mthembu Sithandiwe E. Mazibuko-Mbeje Sonia Silvestri Patrick Orlando Bongani B. Nkambule Christo J.F. Muller Luca Tiano Phiwayinkosi V. Dludla |
| author_sort | Sinenhlanhla X.H. Mthembu |
| collection | DOAJ |
| description | Dyslipidemia is a prominent pathological feature responsible for oxidative stress-induced cardiac damage. Due to their high antioxidant content, dietary compounds, such as aspalathin and sulforaphane, are increasingly explored for their cardioprotective effects against lipid-induced toxicity. Cultured H9c2 cardiomyoblasts, an in vitro model routinely used to assess the pharmacological effect of drugs, were pretreated with the dietary compounds, aspalathin (1 μM) and sulforaphane (10 μM) before exposure to palmitic acid (0.25 mM) to induce lipidemic-related complications. The results showed that both aspalathin and sulforaphane enhanced cellular metabolic activity and improved mitochondrial respiration correlating with improved mRNA expression of genes involved in mitochondrial function, including uncoupling protein 2, peroxisome proliferator-activated receptor, gamma coactivator 1-alpha, nuclear respiratory factor 1, and ubiquinol-cytochrome c reductase complex assembly factor 1. Beyond attenuating lipid peroxidation, the dietary compounds also suppressed intracellular reactive oxygen species and enhanced antioxidant responses, including the mRNA expression of nuclear factor erythroid 2-related factor 2. These envisaged benefits were associated with decreased cellular apoptosis. This preclinical study supports and warrants further investigation into the potential benefits of these dietary compounds or foods rich in aspalathin or sulforaphane in protecting against lipid-induced oxidative damage within the myocardium. |
| format | Article |
| id | doaj-art-0f724dfc622c4c3cb4d6d72fa5435349 |
| institution | DOAJ |
| issn | 2589-9368 |
| language | English |
| publishDate | 2025-03-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Metabolism Open |
| spelling | doaj-art-0f724dfc622c4c3cb4d6d72fa54353492025-08-20T02:57:33ZengElsevierMetabolism Open2589-93682025-03-012510034610.1016/j.metop.2025.100346Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damageSinenhlanhla X.H. Mthembu0Sithandiwe E. Mazibuko-Mbeje1Sonia Silvestri2Patrick Orlando3Bongani B. Nkambule4Christo J.F. Muller5Luca Tiano6Phiwayinkosi V. Dludla7Biomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, 7505, South Africa; Department of Biochemistry, Mafikeng Campus, Northwest University, Mmabatho, 2735, South Africa; Corresponding author. Biomedical Research and Innovation Platform, South African Medical Research Council, PO Box 19070, Tygerberg, 7505, South Africa.Department of Biochemistry, Mafikeng Campus, Northwest University, Mmabatho, 2735, South AfricaDepartment of Life and Environmental Sciences, Polytechnic University of Marche, Ancona, 60131, Italy; Department of Human Sciences and Promotion of Quality of Life, University of San Raffaele, 00166 Roma, Italy; Department of Biomolecular Sciences, University of Urbino Carlo Bo, 61029 Urbino, ItalyDepartment of Life and Environmental Sciences, Polytechnic University of Marche, Ancona, 60131, ItalySchool of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, 4000, South AfricaBiomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, 7505, South Africa; Centre for Cardiometabolic Research Africa (CARMA), Division of Medical Physiology, Stellenbosch University, Tygerberg, 7505, South Africa; Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa, 3886, South AfricaDepartment of Life and Environmental Sciences, Polytechnic University of Marche, Ancona, 60131, ItalyDepartment of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa, 3886, South Africa; Cochrane South Africa, South African Medical Research Council, Tygerberg, 7505, South AfricaDyslipidemia is a prominent pathological feature responsible for oxidative stress-induced cardiac damage. Due to their high antioxidant content, dietary compounds, such as aspalathin and sulforaphane, are increasingly explored for their cardioprotective effects against lipid-induced toxicity. Cultured H9c2 cardiomyoblasts, an in vitro model routinely used to assess the pharmacological effect of drugs, were pretreated with the dietary compounds, aspalathin (1 μM) and sulforaphane (10 μM) before exposure to palmitic acid (0.25 mM) to induce lipidemic-related complications. The results showed that both aspalathin and sulforaphane enhanced cellular metabolic activity and improved mitochondrial respiration correlating with improved mRNA expression of genes involved in mitochondrial function, including uncoupling protein 2, peroxisome proliferator-activated receptor, gamma coactivator 1-alpha, nuclear respiratory factor 1, and ubiquinol-cytochrome c reductase complex assembly factor 1. Beyond attenuating lipid peroxidation, the dietary compounds also suppressed intracellular reactive oxygen species and enhanced antioxidant responses, including the mRNA expression of nuclear factor erythroid 2-related factor 2. These envisaged benefits were associated with decreased cellular apoptosis. This preclinical study supports and warrants further investigation into the potential benefits of these dietary compounds or foods rich in aspalathin or sulforaphane in protecting against lipid-induced oxidative damage within the myocardium.http://www.sciencedirect.com/science/article/pii/S2589936825000027Dietary compoundsAspalathinSulforaphaneCardiac cellsDyslipidemiaMitochondrial function |
| spellingShingle | Sinenhlanhla X.H. Mthembu Sithandiwe E. Mazibuko-Mbeje Sonia Silvestri Patrick Orlando Bongani B. Nkambule Christo J.F. Muller Luca Tiano Phiwayinkosi V. Dludla Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage Metabolism Open Dietary compounds Aspalathin Sulforaphane Cardiac cells Dyslipidemia Mitochondrial function |
| title | Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage |
| title_full | Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage |
| title_fullStr | Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage |
| title_full_unstemmed | Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage |
| title_short | Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage |
| title_sort | supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia associated oxidative damage |
| topic | Dietary compounds Aspalathin Sulforaphane Cardiac cells Dyslipidemia Mitochondrial function |
| url | http://www.sciencedirect.com/science/article/pii/S2589936825000027 |
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