Abstract Rooibos extracts, including its derived polyphenolic compounds, are increasingly explored for their ameliorative effects against diabetes-associated complications. An extract of ‘fermented’ (oxidized) rooibos (FRE) can protect cardiomyocytes from diabetic rats against oxidative stress-induced damage, however, its mechanism of action remains unknown. Using an established model of H9c2 cardiomyocytes exposed to high glucose concentrations, the current study elaborates on mechanisms associated with the cardioprotective effects of FRE, especially its impact on mitochondrial energetics and capacity to enhance intracellular antioxidants under hyperglycemic conditions. The results showed that exposure of H9c2 cardiomyocytes to elevated glucose concentrations induced a state of myocardial substrate inflexibility, characterized by altered free fatty acid (FFA) uptake and oxidation, followed by impaired mitochondrial energetics and accelerated oxidative stress-induced cardiac damage. Our data revealed that FRE ameliorated high glucose-induced abnormalities to a similar degree as metformin. Here FRE treatment improved FFA utilization and enhanced levels of intracellular antioxidants such as glutathione and superoxide dismutase. These are the first results to show that FRE can control cardiac mitochondrial energetics under stimulated hyperglycemic conditions. Of significant interest was the ability of FRE to enhance intracellular coenzyme Q9 levels, a major component of the electron transport chain that plays a crucial role in maintaining efficient aerobic respiration and counteracting oxidative stress. The current results enhance our understanding of the potential protective properties of FRE against high glucose-induced cardiac damage, and also provides impetus for more studies to investigate the modulatory effect of FRE on mitochondrial-linked pathological abnormalities.

中文翻译：

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发酵的路易波士提取物通过改善线粒体能量和细胞内抗氧化能力来减轻高血糖引起的心肌氧化损伤

摘要 Rooibos 提取物，包括其衍生的多酚化合物，越来越多地探索其对糖尿病相关并发症的改善作用。“发酵”（氧化）路易波士 (FRE) 的提取物可以保护糖尿病大鼠的心肌细胞免受氧化应激引起的损伤，但是，其作用机制尚不清楚。使用暴露于高葡萄糖浓度的 H9c2 心肌细胞的既定模型，当前的研究详细阐述了与 FRE 心脏保护作用相关的机制，特别是其对线粒体能量学的影响和在高血糖条件下增强细胞内抗氧化剂的能力。结果表明，H9c2 心肌细胞暴露于升高的葡萄糖浓度会导致心肌底物不灵活状态，其特征是游离脂肪酸 (FFA) 摄取和氧化发生改变，随后线粒体能量受损，氧化应激引起的心脏损伤加速。我们的数据显示，FRE 在与二甲双胍相似的程度上改善了高血糖引起的异常。在这里，FRE 处理提高了 FFA 的利用率，并提高了细胞内抗氧化剂（如谷胱甘肽和超氧化物歧化酶）的水平。这是第一个表明 FRE 可以在受刺激的高血糖条件下控制心脏线粒体能量的结果。令人感兴趣的是 FRE 提高细胞内辅酶 Q9 水平的能力，这是电子传递链的主要组成部分，在维持有效的有氧呼吸和抵消氧化应激方面起着至关重要的作用。