Oxidative stress has been shown to be the main cause of protein denaturation and cell death. However, the exact mechanism of antioxidants against oxidative stress-mediated protein damage and cell cytotoxicity remains largely unknown. Therefore, in this paper, the protective effects of acteoside against HO-inudced hemoglobin structural changes and cardiomyocyte toxicity as models were determined by different techniques. Fluorescence quenching as well as molecular docking simulation studies showed that acteoside potentially interacted with hemoglobin in a one: one binding mode mediated mainly by the involvement of hydrophobic forces. It was also shown that HO caused significant changes in the structure of hemoglobin as well as heme degradation, reversed by acteoside. Additionally, UV–visible studies exhibited that acteoside decreased the generation of methemoglobin triggered by HO Cellular assays displayed that acteoside could mitigate the cardiomyocyte toxicity induced by HO through regulation of LDH release, generation of reactive oxygen species (ROS) and 3,4-methylenedioxyamphetamine (MDA), mitochondrial membrane potential (MMP) collapse, as well as superoxide dismutase (SOD), catalase (CAT), caspase-9, and caspase-3 activities. In conclusion, acteoside may hold great promise for the control of protein-related disorders as well as cardiovascular diseases.

中文翻译：

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类叶升麻苷对生物系统的抗氧化特性：血红蛋白和心肌细胞作为潜在模型

氧化应激已被证明是蛋白质变性和细胞死亡的主要原因。然而，抗氧化剂对抗氧化应激介导的蛋白质损伤和细胞毒性的确切机制仍然很大程度上未知。因此，在本文中，通过不同的技术确定了毛叶升麻苷对 H2O2 引起的血红蛋白结构变化和心肌细胞毒性的保护作用。荧光猝灭以及分子对接模拟研究表明，类叶升麻苷可能与血红蛋白以一对一的结合模式相互作用，主要通过疏水力的参与介导。研究还表明，H2O 引起血红蛋白结构的显着变化以及血红素降解，而类叶升麻苷可逆转这种变化。此外，紫外-可见光研究表明，麦角叶苷可减少 H2O2 引发的高铁血红蛋白的产生。细胞检测表明，麦角叶苷可通过调节 LDH 释放、活性氧 (ROS) 和 3,4-亚甲二氧基安非他明的生成，减轻 H2O2 诱导的心肌细胞毒性。 (MDA)、线粒体膜电位 (MMP) 崩溃以及超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT)、caspase-9 和 caspase-3 活性。总之，麦角叶苷在控制蛋白质相关疾病以及心血管疾病方面可能具有广阔的前景。