Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan, R.O.C.
Division of Cardiac and Vascular Surgery, Cardiovascular Center, Taichung Veterans General Hospital, Taichung, Taiwan, R.O.C.
In Vivo. 2021 Jan-Feb;35(1):155-162. doi: 10.21873/invivo.12243.
BACKGROUND/AIM: Arsenic trioxide (AsO) is an environmental pollutant. However, the detailed mechanisms about AsO-induced loss of endothelial integrity are unknown. This study aimed at investigating how AsO causes endothelial dysfunction and whether baicalin can reverse such dysfunction.
Human umbilical vein endothelial cells (HUVECs) were used to examine AsO-induced oxidative stress, and apoptosis. The influence of baicalin on AsO-induced endothelial dysfunction were investigated.
The viability of HUVECs was inhibited by AsO and cells underwent apoptosis. AsO 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 AsO-induced apoptosis and AsO-suppressed cell viability. Baicalin caused a decrease in NADPH oxidase activity, and re-balanced the ROS level. AsO-induced formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were down-regulated.
Baicalin was found to have the potential capacity to protect endothelial cells from AsO-induced cytotoxicity.
背景/目的:三氧化二砷(AsO)是一种环境污染物。然而,AsO 诱导内皮完整性丧失的详细机制尚不清楚。本研究旨在探讨 AsO 如何引起内皮功能障碍,以及黄芩苷是否可以逆转这种功能障碍。
用人脐静脉内皮细胞(HUVEC)来检测 AsO 诱导的氧化应激和细胞凋亡。研究了黄芩苷对 AsO 诱导的内皮功能障碍的影响。
AsO 抑制 HUVEC 的活力并诱导细胞凋亡。AsO 处理增加了 NADPH 氧化酶的活性,增加了活性氧(ROS)的水平。积累了嘧啶二聚体 DNA-糖苷酶和内切酶 III 可消化的加合物。黄芩苷逆转了 AsO 诱导的细胞凋亡和 AsO 抑制的细胞活力。黄芩苷降低了 NADPH 氧化酶的活性,重新平衡了 ROS 水平。AsO 诱导的嘧啶二聚体 DNA-糖苷酶和内切酶 III 可消化的加合物减少。
发现黄芩苷具有保护内皮细胞免受 AsO 诱导的细胞毒性的潜力。