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. 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.