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Abstract Title:

Protective Effects of Crocetin on Arsenic Trioxide-induced Oxidative Stress in Human Umbilical Vein Endothelial Cells.

Abstract Source:

In Vivo. 2021 Nov-Dec;35(6):3157-3163. PMID: 34697146

Abstract Author(s):

Chung-Lin Tsai, Chia-Wen Tsai, Wen-Shin Chang, Jiunn-Cherng Lin, Liang-Chun Shih, Jie-Long He, DA-Tian Bau

Article Affiliation:

Chung-Lin Tsai

Abstract:

BACKGROUND/AIM: The clinical use of arsenic trioxide (AsO) is hampered due to its cardiotoxicity. Therefore, it is critical to prevent AsO-induced loss of endothelial integrity. The purpose of this study was to examine AsO-induced endothelial dysfunction and evaluate the efficacy of crocetin on reversing AsO-induced cardiotoxicity.

MATERIALS AND METHODS: Cultured human umbilical vein endothelial cells (HUVECs) were used to examine AsO-induced oxidative stress, apoptosis, production of reactive oxygen species (ROS) and DNA adducts. In addition, the impact of crocetin on AsO-induced cardiotoxicity was evaluated.

RESULTS: AsOdecreased the viability of HUVEC cells and led to apoptosis. Additionally, AsOelevated NADPH oxidase activity, and the levels of intracellular ROS. Furthermore, the formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were induced by AsOCrocetin treatment reversed the AsO-induced reduction in cell viability, the induction of apoptosis, the activation of NADPH oxidase activity, ROS levels and DNA adducts.

CONCLUSION: Crocetin protects from AsO-induced cardio-toxicity.

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Sayer Ji
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