The potential protective effect of tricetinidin as novel antioxidant is investigated and compared with selected known antioxidant substances in vitro. Dihydroethidium staining was performed to detect intracellular ROS formation and the protective effect of the antioxidant substances in combination with the superoxide-inducer antimycin a (AMA). Glutathione level, mitochondrial membrane potential and HO-1 expression were analysed for further characterization of the cellular response. The cytokinesis block micronucleus test was applied to investigate the anti-genotoxic effect of the substances against insulin induced genomic damage. AMA treatment caused a significant increase in intracellular ROS formation and insulin treatment induced a significant micronucleus induction in NRK cells. Combination of the antioxidant substances with AMA or insulin protected from the oxidative stress and the micronucleus-induction. All analysed antioxidants showed comparable effects on GSH production and mitochondrial membrane potential. Only delphinidin and tricetinidin caused an increase in HO-1 expression. Tricetinidin and delphinidin might be good candidates for development as an antioxidant supplement. Further research is necessary to show possible therapeutic and preventive effects of tricetinidin and delphinidin in vivo.

研究了tricetinidin作为新型抗氧化剂的潜在保护作用，并与选定的已知抗氧化剂进行了体外比较。进行二氢乙锭染色以检测细胞内ROS的形成以及抗氧化剂与超氧化物诱导剂抗霉素a（AMA）结合的保护作用。分析了谷胱甘肽水平，线粒体膜电位和HO-1表达，以进一步表征细胞反应。胞质分裂阻滞微核试验用于研究该物质对胰岛素诱导的基因组损伤的抗遗传毒性作用。AMA治疗引起细胞内ROS的形成显着增加，胰岛素治疗引起NRK细胞中显着的微核诱导。抗氧化剂与AMA或胰岛素的组合可防止氧化应激和微核诱导。所有分析过的抗氧化剂对GSH生成和线粒体膜电位均显示出可比的影响。仅飞燕草素和tricetinidin导致HO-1表达增加。Tricetinidin和delphinidin可能是抗氧化剂补充剂的良好开发候选物。有必要进行进一步的研究以显示曲克西汀和地芬尼汀的可能的治疗和预防作用体内。