Protective Effects of Baicalin on Arsenic Trioxide-induced Oxidative Damage and Apoptosis in Human Umbilical Vein Endothelial Cells.
In Vivo. 2021 Jan-Feb;35(1):155-162. PMID: 33402461
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 AsOcauses endothelial dysfunction and whether baicalin can reverse such dysfunction.
MATERIALS AND METHODS: 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.
RESULTS: The viability of HUVECs was inhibited by AsOand cells underwent apoptosis. AsOtreatment 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.
CONCLUSION: Baicalin was found to have the potential capacity to protect endothelial cells from AsO-induced cytotoxicity.