Mthembu Sinenhlanhla X H, Mazibuko-Mbeje Sithandiwe E, Silvestri Sonia, Orlando Patrick, Nkambule Bongani B, Muller Christo J F, Tiano Luca, Dludla Phiwayinkosi V
Biomedical Research and Innovation Platform, South African Medical Research Council, Tygerberg, 7505, South Africa.
Department of Biochemistry, Mafikeng Campus, Northwest University, Mmabatho, 2735, South Africa.
Metabol Open. 2025 Jan 3;25:100346. doi: 10.1016/j.metop.2025.100346. eCollection 2025 Mar.
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.
血脂异常是导致氧化应激诱导的心脏损伤的一个突出病理特征。由于其高抗氧化成分，诸如阿萨伊因和萝卜硫素等膳食化合物，正越来越多地被探索其对脂质诱导毒性的心脏保护作用。培养的H9c2心肌母细胞是一种常用于评估药物药理作用的体外模型，在暴露于棕榈酸（0.25 mM）以诱导血脂相关并发症之前，先用膳食化合物阿萨伊因（1 μM）和萝卜硫素（10 μM）进行预处理。结果表明，阿萨伊因和萝卜硫素均增强了细胞代谢活性并改善了线粒体呼吸，这与参与线粒体功能的基因（包括解偶联蛋白2、过氧化物酶体增殖物激活受体、γ共激活因子1-α、核呼吸因子1和泛醇-细胞色素c还原酶复合体组装因子1）的mRNA表达改善相关。除了减轻脂质过氧化外，这些膳食化合物还抑制了细胞内活性氧并增强了抗氧化反应，包括核因子红细胞2相关因子2的mRNA表达。这些预期的益处与细胞凋亡减少有关。这项临床前研究支持并值得进一步研究这些膳食化合物或富含阿萨伊因或萝卜硫素的食物在预防心肌脂质诱导的氧化损伤方面的潜在益处。
