Background/Aim: Arsenic trioxide (As2O3) is an environmental pollutant. However, the detailed mechanisms about As2O3-induced loss of endothelial integrity are unknown. This study aimed at investigating how As2O3 causes endothelial dysfunction and whether baicalin can reverse such dysfunction. Materials and Methods: Human umbilical vein endothelial cells (HUVECs) were used to examine As2O3-induced oxidative stress, and apoptosis. The influence of baicalin on As2O3-induced endothelial dysfunction were investigated. Results: The viability of HUVECs was inhibited by As2O3 and cells underwent apoptosis. As2O3 treatment increased NADPH oxidase activity, and elevated the level of reactive oxygen species (ROS). Formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were accumulated. Baicalin reversed As2O3-induced apoptosis and As2O3-suppressed cell viability. Baicalin caused a decrease in NADPH oxidase activity, and re-balanced the ROS level. As2O3-induced formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were down-regulated. Conclusion: Baicalin was found to have the potential capacity to protect endothelial cells from As2O3-induced cytotoxicity.

中文翻译：

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黄芩苷对三氧化二砷诱导的人脐静脉内皮细胞氧化损伤及凋亡的保护作用

背景/目的：三氧化二砷 (As2O3) 是一种环境污染物。然而，关于 As2O3 诱导内皮完整性丧失的详细机制尚不清楚。本研究旨在调查 As2O3 如何导致内皮功能障碍以及黄芩苷是否可以逆转这种功能障碍。材料和方法：使用人脐静脉内皮细胞 (HUVEC) 检测 As2O3 诱导的氧化应激和细胞凋亡。研究了黄芩苷对 As2O3 诱导的内皮功能障碍的影响。结果：As2O3抑制HUVECs的活力，细胞发生凋亡。As2O3 处理增加了 NADPH 氧化酶活性，并提高了活性氧 (ROS) 的水平。甲酰胺嘧啶 DNA-糖基化酶和内切核酸酶 III 可消化的加合物被积累。黄芩苷逆转 As2O3 诱导的细胞凋亡和 As2O3 抑制的细胞活力。黄芩苷导致 NADPH 氧化酶活性降低，并重新平衡 ROS 水平。As2O3 诱导的甲酰胺嘧啶 DNA-糖基化酶和内切核酸酶 III 可消化的加合物被下调。结论：黄芩苷被发现具有保护内皮细胞免受 As2O3 诱导的细胞毒性的潜在能力。